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·VENOUS RETURN ·FRONTISPIECE FICE RF 1 Illu tration of the expan son of an and sepse Interior view of the etpo ed heart and great res els during cris ne the le cent of the atrioventricular junction luring ventricular drastolc B = The same sick during sentricular catricular systole It can be seen how ventricular contruction tole Dms og bs Rollet ISSO (Hermanns Handbook of might Iru I look into the atrın by espin ling them I lussuology) after an original by Henke 1872

·VENOUS RETURN
by
GERHARD A BRECHER, MD, PhD
Julius | Stone Profes or of Physiology Depart
ment of Physiology College of Medicine The Ohio
Staic Unncrsity Columbus Ohio
GRUNE & STRATTON
New York
1956
London
mm
C!! 15 st

·Library of Congress Catalog Card No 56-9121
Copyright 1926
GRUNE & STRATTON I c
381 Fourth Avenue
New York 16 NY
Printed and I nun in USA for Gaur STRATTON

·Contents VI 1 1 1 3 Foreword by Carl J TI 1ggets Preface I Historical Considerations V 13 & tergo Vis a fronte during ventricular diastole 13 a fronte during ventricular sy tole Static negative intrathoracic pressure Re piratory movements II Elementary llemodynamics Poi euilles law Terminolog of va cular pre cures III Factors Affecting I enous Return Effect of gravity on venous return Venous valves Venous distensibility and tone Mers ous and humoral regulation Il Present Problems of Venous Return Dynamics enous collap e phenomena Controversial effect of re piration The heart as a factor in venous return V Methods for Venous Flow Veasurement Venous drainage recorders Pecording of pulsatile flow Pecent des elopments Critique of differential pressure flow meters Pendulum flowmeters Critique of pendulum flow meters Other phasic flow meters Izdırect methods VI I enous Hemodynamics Vodification of Poi cuilles las Pres ure gradient along central veins Pres ure flow relations in collapsible ves els Significance of venous collapse in the peripheral circulation The mu cle pump without valves VII The Respiratory Pump Time factor in venous collapse Effect of re piratory movements on superior caval flow Iofluence of respiration on inferior caval flow Pespiratory variations of portal for Respirogenic changes of total venous retum 8 11 11 12 13 10 19 21 22 26 26 27 27 30 30 31 39 10 12 18 19 al 51 57 6) 71 71 71 76 8.3 81 Y ·TENOUS RETURN Region of venous collapse during inspiration Clinical infcrences VIII Cffect of Artificial Respiration on 1 enous Return Flon in normos olemia Flow in hypov olemta Venous return in the open chest Venous return and cardiac output during artificial respiration Flow during lung inflation in the open chest Clinical implications I\ Effect of the Heart & Action on 1 enous Return Central venous flow pattern The active ventricular systole Venous return during ventricular diastole Phasic infion and strohe solume during natural breathing Acwer concepts of the hearts action on cnous return I l cnous llcmodynamics of Cardiac I alie Lesions Mitral and tricuspid insufficiencies Alitral and tricuspid stenoses Pericardial effu ion I Tenous Retun During Cardiac Surgery Closed heart surgery Open heart surgers rinal Remarks Bibliography Index 85 89 91 91 9 9a 97 99 100 101 101 101 107 110 112 115 113 118 119 121 122 123 128 129 141 ·Foreword It is axiomatic that the heart can pump only as much blood as it receives! Indeed the volume of blood returned to the heart is the ba ic determinant of cardiac output Since the latter varies enormously under ordinary conditions of daily activity the mechanı ms that facilitate venous return have been the subject of di cussion for centuries During the past two decades the application of physical principles the u e of hemodynamic models and fragmentary tudies on man and animals have brought to light many factors that favor or hinder venous return It has proved difficult however to harmonize differing conclusions and to integrate them into a phy iological mechan; m applicable to the intact body The state of confusion that has existed during the past two decades has been partly duc to the lack of adequate metering devices applicable to the vena caval systems For this reason a number of optically recording phasic flowmeters suitable for use in venous systems were designed in the Physiological Laboratory of Western Reserve Unit crsity Medical School Some of these were constructed under the guidance of Dr Brecher and in 1933 there eventuated the high fidelity electronic bristle flow meter of Brecher and Praglin The development of new and u eful instruments is itself a commendable ac complishment But real progress is made only through their application to cogent problems by competent and di cerning investigators Fortunately Dr Brecher po se es both inventive talents and zeal for personal participation in experi mental work The pre ent monogr iplı not only presents a comprehensible comprehensive account of Dr Brecher s contributions but al o an excellent historical survey of work preceding his own studies The illustrations are profuse and relevant a large number are original All add materially to the presentation It will be obvious to the reader that Dr Brecher has applied both synthetic and analytic approaches to the problem of venous return as nature engineered it in the body rather than setting up physical chemes which would or might accomplı h the same end This monograph is the only current one that gives a comprehensive analysis of the determinants of venous return and its adaptation to cardiac output based on experimental measurement of venous fion It should be welcomed alike by laboratory investigators and clinicians who must at all times be alert to avoid procedures that interfere with natural factors favoring venous return CARL J TIGGERS MD ScD V11

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·Preface It has often been stated that the venous system is the forgotten part of the circulation Although exaggerated this statement is not quite unfounded If the amount of emphasis placed on a cubject taught in medical school could be used as a yardstich the venous system would appear to be of minor in portance The lecturer usually takes refuge in the consolation that relatively little concrete and noncontroversial information is available about the return flow of blood in the veins A treatise on this subject appears desirable because no comprehensive work on the venous system has been published since henneth J Franklins A Mono graph on Veins in 1937 The present book is not intended to survey the entre field of venous physiology and anatomy since 1937 as Franklin s monograph does up to that date Its scope is more limited It will deal specifically with the dynamic aspects of the return flow of blood to the heart These functional aspects become increasingly the focus of interest in basic research and clinical thinking since it is not the static pressure of blood in a circulatory bed (as reflected by pressure measurements) but rather the movement of blood which is of biological importance for the exchange of metabolites and fudi in the tissues For this reason special emphasis will be placed in this monograph on the effect of heart action and respiration on venous flow dynamics In addition to Franklin a book I wish to refer to other accounts of certain aspects of the venous system whose contents I have not intended to duplicate The reader should consult them for information on the specific problems treated there The basic principles of correlation in the circulatory system are enun ciated in the article Venensystem und Kreislaufregulierung (1932) by the late Llothilde Gollwitzer Meier A detailed study of venous flos dynamics with the aid of X ray cinematography is reported by W Bohme in the account Uber den aktiven Anteil des Herzens an der Forderung des Venenblutes (1936) Landis and Horten tine have emphasized the interrelation of venous pressures and fuid exchange in their review on Functional Significance of Venous Pres sure (1950) Two books of G E Burch A Primer of Venous Pressure (1950) and Digital Plethysmography (1954), deal with the methods and clinical applications of venous pressure measurements and of plethysmographic flow recordings respectively I am particularly indebted to all my associates and friends in the Depart ment of Physiology at Western Reserve Universit: Cleveland Ohio where much of the experimental work reported in this book was done Dr Carl J Wiggers was a source of continuous inspiration and helpful criticism while I had the privilege of working in his famous cardiovascular laboratory I wish to thank especially Drs Emil Ritter George Mixter Jr Julius Praglın Charles A Hubay and EQ Adams for the large part they played in the studies of venous flow, and Mr Clyde Bratton Mr Richard Frecmun Mr Villard Stires 18 ·X IEVOLS RETLRY ind Nir Eugene Scott for their technical a aistance Several members of the physiology departments at lle tern Reserse University and Olno State Uni versity have htlped in the preparation of the manuscript by their valuable uggestions Van friends in different parts of the world harc liberally con tributed by lending me originals of illustrations Although all are not men tioned individually I thank miery one I also want to achnon ledge with many thanks the valuable support of the Life Insurance Vedical Research Fund, the Cleveland Arca Heart Society and the Imerican Heart Association for making this work posible (CRIIRD A BRECHER Columbus Ohio January 1956 ·Historical Considerations As early as the third century BC, thought was given to the question of how blood enters the hcart At that time the Greeh physician Erasıstratus is sup posed to have stated that the heart acts as a pressure suction pump sucking blood into the ventricles during diastole Ever since that time and even after the days of Sır 11 illiam Harvey, the opinion has been voiced that the force imparted by the heart to the expelled blood is not sufficient to explain venous return and filling of the ventricles The nature of other forces which bring about the return flow of blood to the heart has been the subject of heated discussion and controversy for centuries Even today opinion is far from uniform Probably the main reason why knowledge of venous return has not hept pace with our understanding of the other parts of the circulatory system is the lack of adequate methods for accurate measurements of venous flow Each time a new idea and methodological approuch was advanced which helped to explain some a pect of venous return it gave a new impetus to inve tigative endeavors Numerous simple experiments and deductions have been forgotten only to be redi covered by more advanced and comphcated methods Since the effect of the hearts action and respiration on venous return are the subjects of particular interest for an under tanding of venous flow dynamics the historical considerations are confined to these problems VIS 4 TERGO The propelling force which is imparted by the myocardial contraction to the blood during its pa sage through the heart is called the ris a tergo This force from behind even after its reduction in the arterioles and capillaries is be lieved to be sufficient to account for an adequate return flow of blood This view was first clearly cypressed by Harvey in 1628 It was quickly accepted by scientists as documented by Loner who wrote in De Corde' (1669) It is an undisputed fact that the return of the venous blood is the result of the impulse olen to the arterial blood and not of any attraction by the heart" Even up to the present the authority of Harvey has greatly contributed to the persistence of the vie that the heart acts etclusively as a pressure pump A number of cla sical experiments are usually quoted (Poiseulle, 1830 Ledder hose 1906) to prove that in the absence of other forces (muscular contractions respiration and hydrostatic differences) blood is adequately returned to the heart by the vis a tergo However these experiments cannot be considered as conclusive evidence that the 123 a tergo is the ole cause of the return fion of blood in the ab ence of mu cular respiratory and hydrostatic factors If the heart by its contraction and relaxation should in some way or another attract the venous blood it could augment venous return Unfortunately this suching force cannot be casily distinguished from the pure ris a tergo when the effects of respiration the mu cle pump or hydrostatic pressure are eliminated ·2 VENOUS RETURN Summar ing The vis a tergo appears to be the main but not the sole force responsible for the return flow of blood VIS A FROVTE DURING VEYTRICUL IR DIASTOLE The force or combination of forces acting from the front to attract blood in the veins towards the heart is called the vis a fronte This force may stem from the action of the heart itself or from the action of the respiration Let us first consider the opinions about the vis a fronte which may be attributed to the heart The view of Erasistratus (c 290 BC) and later of Galen of Pergamon (131- 201 AD) that the heart is a pressure suction pump was founded mainly on the assumption that blood was sucked into the ventricles by their active en largement Galen believed that the heart contamned muscles which spread the ventricular walls apart after their systole We are inclined to smile about this "naive misconception of Galen, whoso opinion determined and confused scien tific thinking for 1300 years up to the Renaissance But was he really so com pletely mistaken? The most recent authority on the subject Guasp (1954) mahes a very good (though not experimentally proven) case for the existence of specific musculature in the heart thich actuelv evpands the ventricular cavities at the beginning of diastole He states "The force that expands the ventricles is represented by the intramural conducts and by the muscular trabeculae which form the 3 entricular spongy system In the 2300 years be tween Erasistratus and Guasp opinions have varied and clashed between the two extremes, ze between the adherents of an actre diastolo and thosc assum ing a purely passive role of the ventricle in diastole The older literature was extensively reviewed by Ebstein (1901) Undoubt edly Harvey was the first scientist of modern times who denied the existence of an active diastole nhen he wrote in 1628 "Likewise, it is not true as commonly believed, that the heart by its own action or distension draws blood into its ventricle The father of physiology, Albrecht von Haller (1708-1777), also did not believe that the heart exerted a sucking action On the other hand, Zugenbuhler (1815) and Schubarth (1817) argued that the ventricles must such blood into their cavities to preient the formation of an "empty space The first experimental approach to the subject was made in 1828 by Wcde moyer who inserted a catheter into the jugular vein of a horse He observed during atrial diastole a rise of colored fluid in a glass tube attached to the end of the catheter Wedemey er interpreted this as a sucking action of the heart on the blood in the casal reins during the diastole of the atria and called it atrial aspiration Donders (1859) believed that WVcdemey er's observation speal s strongly in favor of an active expansion of the heart but that it does not prove it conclusively The idea of an atrial aspiration has not been abandoned even in modern times Based apparently on Il edemey er s observation, we find in the 1955 edition of Houssay s textbook Human Phreiology the statement that the heart asserts a certain sucking effect on the blood of the veins at the beginning of auricular diastole No conclu ions as to the action of ventricular ·diastole can be arrived at from Wedemey er s esperiments because atrial diastole comprises the period of sentricular sy stole and beginning of sentricular diastole Goltz and Gaule (1878) swung the pendulum of opinion strongly to the side of ventricular aspiration They reported that pressures fell during diastole in the left ventricle to -52 mm Hg in the right ventricle to -172 mm Hg and in the right atrium to -112 mm Hg In the opinion of most scientists the hypothesis of a distolic ventricular aspiration became untenable after the advent of modern manometry based on the sound physical principles advocated by Otto Frank Von den Velden (1906) Straub (1910) and Wiggers (1928) showed with manometers of high frequency response that Goltz's recordings of negative pressures were caused by instru mental errors Nevertheless the battle continued even in CJ Wiggers own laboratory when hatz (1930) observed a marked diastolic sucking action of the ventricle Working in the same laboratory, Cotton (1934) pointed out only four years later that it was hatz s experimental arrangement and not the heart that may have been responsible for the apparent sucking action The latest contributions in favor of an active diastole are from Villa (1954) Guasp (1954) and Cignolını (1954) Though working independently thesc authors have come to similar conclusions, based on theoretical considerations and inferential evi dence The active dilatation of the heart muscle has been attributed to various forces First some believe that a portion of the myocardium expands the ventricular cavity by contraction of its musule fibers at the beginning of diastole The action of these fibers would be antagonistic to those which cause the expulsion of blood from the ventricles (Galen Brauer (1904] Guasp (1954] This view was opposed by Hyrtl who stated in 1855 In the heart there is not a single muscle bundle pre ent which by its contraction could enlarge the cardiac cavities Second a group of workers represented by Donders (1859) believed that the blood which enters at the end of systole into the coronary arteries seems to cause a slight active expansion of the heart especially of the ventricles' This view was formulated by Bruche in 1855 (see 1872) and particularly advocated by Lucianı (1911) A modification of this hypothesis is presented by Cignolını (1954) based on x ray kymograph studies Third some have attributed the aspiration of the heart during diastole to the recoil of elastic elements or an active de contraction of the muscle Adherents of this view include Magendie (1817) Lucianı (1911) Goltz and Gaule (1878) and Villa (1954) Summariwing Though the ancient by pothesis of a diastolic aspiration of blood by an ex pansion of the ventricular cavities has gradually lost ground, several arguments in favor of this hypothesis have never been conclusively proven or disproven under properly designed experimental conditions VIS A FRONTE DURING VENTRICULAR SYSTOLE Bohme (1936) pointed out that one could consider Aristotle (384-322 BC) as the first who mentioned a process which may affect venous return during ventricular systole Aristotle is credited with the discovery of the punctum saliens re, the observation of alternating cardiac volume changes in the bird ·ENOUS RETUR embryo As Benninghof showed cinematographically in 1935, the movement of the atriot entricular junction during ventricular sy stole in birds corresponds closely to that observed in mammalian hearts The idea that the contraction of the ventricular muscle during systole could attract blood in the seins toward the heart has appcaled to scientists far less than the diastolic aspiration No mention of it is made in the classical cardio Vascular literature until Purhinje in 1843 and Nega in 1852 hs pothesized that the heart cxerts a sucking action during systole Purkinje noted that the apex of the bcating heart mores relatively little (he called it punctum firum) whereas the atrioventricular junction moves, during ventricular systolc, relatively greatly toward the ape (he called the atrioventricular junction the punctum mobile) Functionally inclined anatomists who observed form changes of the heart dur ing its cycle became the main proponents of this theory, which has only re cently aroused the interest of phy 1ologists The manner in which the contracting ventricle is supposcd to draw blood from the vcins into the atria is best illustrated by the original dran ing of the anatomist Honhe They are reproduced in Fig 1 (A and B) Hedren these schematic diagrıms in 1872 from direct observations on In ng animals in Carl Ludvigs famous cardiovascular laboratory and from autopsy material These figures cxplain better than words the form changes of the heart which sugge t 1 systolic attraction of blood Rollct nho produced Henke's drawings in Hermans llandbooh of Physiology, stated 'One can seu hon during ventricular sy stole the atrios entricular junction an proaches the ape which remains almost stationary hercas during diastole the atrioventricular junction returns to its previous position This descent and ascent of the atrioventricular junction is the most conspicuous mouement which can be perceived in the acting heart' He believed that blood is suched into the atria by the descent of the atriosentricular junction and that the lungs by their clastic pull und in maintaining the outer contour of the atria Apparently this hypothesis soon drifted into oblivion since no evidence other than the observation of the heart s movement could be marsh alled in support of the systolic suction However, some interest was maintained by another group of investigators Clinicians and physioloists who attempted to interpret minute fluctuations of air pressure in the respiratory channels as due to changes in the volume of the heart (cardio pneumogram) found in the complex pattern of their tracinge cer tun deflections which could be interpreted as 1 systolic suction of the ventricles In 1832 Cerıdını recorded cardio pneumograms from a hich he de cloped formu lae for the calculation of cardiac output The extensic literature on this subject has been resica cd by Hamilton (1930) and Holzlohner (1932) These tho authors came independently to similar con clu ions Hamilton deduced from human cardio pneumograms that atrial oflon during sentricul ir sy stole could be almost as large as the ventricular stroko volume Holzlohner, who used a hot wire anemometer, concluded that "the ve nous blood inflow becomes stronger than the arterial discharge during the second part of the outflos period of the left ventricle" He later added (1936) that for

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·HISTORICAL CONSIDERATIONS 7 The static position of the thorau would be best defined as that assumed during the normal cipiratory pause Pfuhl calculated in 1929 from incasurements of the total surface area in man that in this position the retractive force of the lungs was 15 to 20 hg The retractic force acts through the pericardium on the heart It was calculated as 048 kg acting on the entire surface area of the right atrium 1 73 kg on the right ventricle, 01 Kg upon the left atrium and 0 96 hg on the luit vcntricle Following the ideas of Carson Barry and Donders Pfuhl believed that the continuous lung traction is the inout inportant factor for the filling of the atria and ventricles by holding them opon 11hcn the myocardium contracts part of the cnergy must be used to overcome the lung traction which is the permanent dilator of the heart chambers The atrial muscle may not contract to the samc cxtent in the closed as in the open chest because lung traction opposes the atrial contraction Continuous lung traction holds the intrathoracic veins and hcart chambers open and creates a low pressure in them This causes the blood to flow from the 1egions of lugher pressure outside the thorax into the chest veins and heart Unquestionably the continuous action of lung traction produces a greater pressure difference between the cxtrathoracic capillaries and the heart chambers than would cxist in its absence such as m open thoracotomy However how much this factor alone contributes to a greater venous return is difficult to quantitate since shortly after opening of the thorax compepsatory mechanisms come into play which bring venous rcturn, and thus cardiac output, to nearly the same level an custod in the closed chest The fact that the circulation is well maintained after thc chest is opened has caused today s_physiologuts and thoracic surgeons to minimize the importance of the continuous elastic traction of the lungs on venous return No clarification of the importance of this factor can be obtained until quantitative measurements of venous return in suitable experiments are available The classical view of the continuous elastic traction of the lungs which dilates the heart chambers and counteracts their complete emptying has been recently supported by Rushmer (1954) who used an entirely different approach He inserted 3 strain gauge spring device into the left ventricle and measured the transverse diameter of the left ventricular cavity in dogs with the chest open and closed He found that in the closed chest the left ventricular chamber has a greater diameter during systole and at the end of sy stole than when the lung traction is abolished by opening the chest Though static negative pressure in the thorax tends to hold the heart chambers open it is fallacious to assume that this pressure as such as performng worl The cnergy available from elastic recoil is a potential energy and ex ternal work can only be done when this potential encrgy level is altered Thus kinetic energy can only be released (= work performed) through changes of intrathoracic pressure by muscular activity Summarizing The continuous clastic traction of the lungs creates negatirc intrathoracic presuie and thus favors venous return by producing & pressure difference ·6 VENOUS RETURN of the atrial curities and the de cent of the atrioventricular junction during yentricular sy stole Hc injected diops of iodopin oil into the jugular vein and shoned that during ventricular systole the e drops a.cre greatly accelerated in their flow through the superior vena cas i He stated 'With these observations the proof of the systolic suction attraction (Ansaugung) of the venous blood by the heart appears to be finalls established One can see that during the time when the ventrcle becomes smaller while cjecting its content and the atrium enlarges in the direction toward the retracting entriele both venac cavao de crease in caliber simultaneously with a remarkable centripetal acccleration of their content Since this occurs irrespective of an inspiratory or expiratory po sition of the thorax and even in the absence of any action from the lungs there can be little doubt that a great active participation of the heart in promoting venous return has been finally proven It may appear that Bolime solved the problem However, he himself pointed out that lus obscrvations were of qualitative nature only By comparing the velocity of iodopın oil drops in the caval veins during ventricular systole and diastole he inferred that 10 times as much blood would flow toward the heart during systole as during diastole Holzlohner and Schonerstedt therefore at tempted in 1940 to quantitate with the aid of a flowmeter the amount of blood which flows through the external jugular vein of 4 dog during ventricular sy stole and diastole They believed that Bohme s estimates were too high regarding the portion of the blood which passes through the vem during systole Summari.ing Though relatarely late in its conception the theory of an attraction of venous blood by the contraction of the ventricle has gained greatly in favor It is sup ported by rather inconclusive evidence derived from anatomical observations cardio pneumograms and venous and atrial pressure pulses It is strongly sup ported by qualitative evidence from x ray cinematographic studies STATIC NEGATIVE INTRATHORACIC PRFSSURE One must distinguish between two effects of the respiratory apparatus on cnous return (1) The static effect of the continuous negative intrathoracic pressure and (2) the dynamic effects of changes in intrathoracic pressure which occur during spontancous respiration artificial respiration, controlled respira tion and various voluntary and involuntary respiratory maneuvers Under normal physiological conditions static and dynamic effects are integrated in their action on thc return ilos of blood but they can be separated theoretically and experimentally For many years the opinion presailed that the permanent clastic traction of the lungs is one of the most important causes of venous return by virtue of the production of negative intrathoracic pressure This vies goes back to the carly part of the eighteenth century when the work of Carson Barry Ludwig and Donders on the tractre force of the lungs moved into the center of attention among physicians In the nork of Car on (1820) and Barry (1826) the continu ous cffects of lung traction upon venous return was distinguished for the first time from the intermittent effects produced by respiratory movements ·HISTORICAL COIDERATIONS 9 » though his results were only of a qualitatile nature, the ingeniously conceived experimental arrangement embodies the principles of the more recently de veloped velocity flow meters The results of Barry have gn en rise to a number of questions which have stimulated investigators up to the present (1) Why is the blood flow through the jugular vein during inspiration accelerated only when the horse is lying down? (2) Why did Barry not observe changes of blood flow synchronous with respiration when the horse was standing? (3) What caused pulsatile flow of blood of higher frequency than the arterial pulse? (The answers are dis cussed on pp 66 and 71 ) The classical view concerning the effect of respiratory movements on venous return is be t stated bs Donders (1859) During quiet inspiration and expira tion blood is always drann toward the thoracic cavity with stronger in Spiration it becomes strongly attracted by the chest cavity only in strong ex piration i it pressed out of the thoracic cavity Donders thus introduced the concept of the respiratory pucap It was based on the logical deduction that blood flot ton ard the heart must increase when the intrathoracic pressure becomes lower during inspiration Since no experi mental evidence was presented by him his opinion was subjected to criticism by others as discussed by Henderson and Barringer (1913 a, b) Volkmann (1850) Mono (1878) and Ledderhose (1906) believed that the increased Venous return during inspiration was cancelled by a corresponding reduction of venous return during expiration and as a net result respiratory movements would not increase venous return A number of authors argued that the return flow of blood from the inferior and superior venae cavae either differed greatly or were er en opposite in direction during the respiratory phases T Lewis (1908) and later Eppinger and Hofbauer (1911) thou,ht that inferior caval flow decreased during inspiration On the other hand de Jager (1883) su gested that it must increase on account of the increase in abdominal pres sure Franklin (1937) tahes the view that inferior vena cava flow may be variable as the result of inspiration Seely (1948) could not find any evidence from intracardiac pressure measurements that inspiration augments venous return Golluitzer Veier summarized her opinion in 1932 as follows Venous return is favored in the superior vena cava and in the hepatic veins during inspiration but decreased during espiration in the inferior vena cava and portal ves els venous return is decreased during inspiration but increased during expiration An entirely new aspect was given to this question by the collapse theory' of Holt (1940 1941 1943) and Duomarco (1944 1945 1946 and 1950) On the basis of indirect evidence and of experiments with physical models they concluded that a decrease of intrathoracic pressure cannot influence the inflow of blood into the right atrium The argument of the adherents of the collapse theory way that with the onset of inspiration the great reins collapse at the point where they enter the chest As a consequence of this collapse resistance to flow in the collapsed citrathoracic veins must increase Therefore atrial inflow cannot become greater or may even become less during inspiration In pite of consincing arguments in favor of the collapse theory which were ·10 VENOUS RETURN particularly advanced by Duomarco, an impressiye host of indirect evidence can be marshalled in favor of an increased right atrial inflow with inspiration It was found by Wiggers (1914), Bloomfield (1945), Lauson et al (1946) and Opdyke and Brecher (1950) that right atrial and right ventricular pressures rise with inspiration This pressure rise could be explained by an increase in volume of the right heart, although admittedly it would also be explained by an increase of pulmonary vascular bed resistance (Opdyke et al 1950 Hoffman, 1951) Changes in the atrial and senous pressurc pulse contours under various con ditions have been attributed by Takashima (1953 a b, c, 1954) to a respirogenic increase of venous return Increased sentricular diastolic size, recorded by dif ferential cardiometers (Boyd and Patras 1941) and cinematography also contribute similar presumptive cudence (Shuler et al 1942) Summarizing In the absence of direct evidence, various and controversial opinions as to the effect of respiration on venous return have been voiced The best represented views are the classical theory of Donders according to which venous return increases with inspiration and the new collapse theory of Holt and Duomarco, according to which venous return docs not increase with inspiration ·11 Elementary Hemodynamics Before dealing with the specific aspects of venous flor dynamic a brief review of a few general hemodynamic principles may be of value to those who are not in frequent contact with the subject. (For details consult Lamport [1900] Wiggers (1932]) POISEVILLE'S LAW Hemodynamics is a study of the forces which cau.e alter and regulate the flow of blood through the body In a modified form many physical laws de rived from hydrodynamics are applicable to the flon of blood Generally stated the quantity of blood (Q) passing through the circulatory system or through a part of it increa es with the perfusing pressure (P) and decrea es with the resistance (R) to low, as expressed by the equation Q = P/R In cssence this represents Poiseuille's law for nonturbulent flow through tubes it can be expres ed in greater detail as I'ípi - Q 8n1 In this equation Q = the quantity of flow through a vessel (tube) per unit time 7= 31416 r = radius of the vessel Pi = pressure at an upstream point of the vessel p = pressure at a downstream point of the vessel = coefficient of viscosity and I = length of tube This means that volume flow is enhanced by an increase of any factor in the numerator and diminished by an increase of any factor in the denominator of the formula Each factor must be considered separately for its specific application According to Poiseuilles law the factor which most affects volume flow is the radius of the vessel since it is raised to the fourth power in the formula As illustrated in Fig 2 volume fow through a vessel would increase sixteen times iſ the radius were doubled This relationship between radius and volume flow applies only to rigid tubes or vessels which have a circular cross sectional area such as arteries or full veins Thus the applicability of Poiseuille 8 law is best demonstrated by companog flow through arteries of various calibers or through one artery at various stages of expansion or constriction As is well known the regulation of blood flow in the capillary beds is achieved mainly by increasing or decrea ing the diameter of the artrioles the stopcochs of the circulation we shall see in Chapter 6 that Poiseuille s law has to be modified for application to the venous system because the crossec tional area of veins is usually not circular Blood is caused to flow from one point to another in the vascular bed by the difference of pressure between such points According to Poiseuilles law volume flow becomes greater when the pressure difference (= pressure gra dicnt] (P. - p ]) increases other factors remaining the same Since p is di rectly proportional to flow in Poiseuilles formula flos varies linearly with ·12 VENOUS RETURN r: mm r = 2 mm ICC / SEC 16 CC / SEC А B FICURE” Effect of changes in radius of a vesel on flow The c10 s-sectional uca of the ics.cl is circular lll other factors remaining constant a vessel of 1 mm radius (1) would dis. charge 1 ec scc as compared to 16 cc /scc from a ses cl of 2 mm radius (B) The cros sec tional vea of the 2 mm vessel is four times that of the 1 mm cscl is s iclation of cross sectional area to flow the cxpression is a fourfold increase of the circular cros sec tional aren results in a sixtccnfold increase in volume flow the pressure gradient This means that a doubling of the pressure gradient along the vascular bed will double the amount of blood passing through it For changing thic amount of blood flow, nature mahes less use of altering pressures than of changing the cssels radu The same sixtcenfold increase in blood flow which could be brought about by doubling a vessel s radius would demand an increase of the blood pressure by sixteen times Flow varies in inverse proportion with the length 1, of a vessel Volume flow decreases by one half of the length of a vessel is doubled, other factors remain ing the same Simularly the relationship beta con viscosity and volume flow is a simple reciprocal one Flow would decrease by ono half blood becamo twice as viscous Summari ing Volume flow through the circulatory system or part of it becomes larger with an increase in the radius of a vessel and the pressure gradient along the vascular bed Volume flow decrcascs with an increase in blood viscosity and the length of a vessel TERMINOLOGI OF VASCI LAR PRESSURES What is ordmarily called blood pressure is the lateral pressure of blood on the wall of 1 sc sel It is determined by the volume clasticity of the systein It can cut in a clo cd system whethier blood is stagnant or in motion Ls en after ce ation of all blood flos (eg after cardiac arrest) the volume of blood contained in the vascular bcd exerts on the walls of the scssel a pressure which comes to an equilibrium in all arteries and icin This pressure amounts to about 6 rum ll, in do, and is called variously mcan systemic pressure, tatic ·ELCIEVTAR) IEVODI NAMICS 13 blood pressure' or lately, "mean circulatory filling pre-sure" (Guyton et al 1954) The pressure in a vessel 29 measured directly by inserting a cannula and connecting it to a manometer at the same hydrostatic level as the vessel If the vessel is exposed to the atmosphere the intralascular pressure is measured against the atmospheric pressure Most ves els are however, imbedded in tissues which have 4 certain tissue pressure that is either hgher (eg, in the abdomen) or loser (eg in the thorax) than the atmospheric pressure For accuracy, the intravascular pressure should thcrefore, be measured against the extravascular (tissue) pressure which surrounds the vessel Burton has introduced the term "transmural pressure" to characterize the pressure measured ins of a vessel as related to that wurrounding at and Yamada, 1951) Transmural pressure is defined as the pressure difference between the intravascular and extravascular pressure This is the pressure gradient across the vessels wall (inside ininus outside pressure) It should be emphasized that the transmural pressure defined as the pressure giadient across the wall of a vessel refers only to the lateral pressure it a given point of a vessel This must not be confu cd with the pressurc gradient which clists along the vascular bed that is, between an upstream and downstream point (p - p) in Poiseuilles formula Only the latter is re ponsible for the movement of blood along the channels of the circulatory system Recently difficulties have arisen in terminology because of the similarity in usage of the term effective pres ure and transmural pres ure' Originally when Henderson (1909) and Hender on and Barringer (1913) introduced the term effective pressure they used it to mean the pres ure which affects the filling of the heart ( effective filling pressure ) In their thinking effective pressure combined both the pressure gradient across the vessel wall (vena caval minus intrathoracic pressure) and the pressure gradient along the vascular bed (pressure difference between vena caval and intraventricular diastolic pressure the difference which is responsible for the flow of blood from the (aval veins into the right ventricle) Recent usage of this term does not quite coincide with Hender ons original meaning eg Setly 1918 Opdyhe ind Brecher 1900 Opdyl e ct al 1950 Duomarco et al 1950 Alexander 1901 and Coleridge and I inden 1994) As u ed by these authors the effective pressure has become 1 term for intravascular pressures in relation to extravascular pressures Used in this way the 'effective has lost its original significance and has acquired the same meaning as transmural pressure Cournand and his group circumvent terminological difficulties by calling the effective pre sure net pressure In this bool the term transmural pres ure will be used prefer entially because it is clearly defined and has no varying connotations The difficulties in determining transinural pressure are mainly technical Except for very small vessels the intravascular pressure can be measured di rectly Hotever the determination of extravascular pressure 18 quite unreliable The greatest artifacts are encountered in measuring tissue pressure in relatively (Swann et al 1950) and the least recording the pressure which surrounds the great rescels and heart Intrathoracic pressure can be taben as the best approximation for the latter Even o calculations of transinural pres solid or ·14 IE. VOUS RETUR sure in the heart cavities and large vessels hinge on the critical measurement of intrathoracic pressure in closest proximity to the place of intraluminal pres sure measurement since intrathoracic pressure is not uniform in all parts of the chest (Viggers et al, 1947) This was again emphasized and critically reviewed by Coleridge and Linden (1954) Summarizing For greater accuracy the intravascular pressure exerted on the wall of a vessel is not measured against atmospheric pressure, but against the tissue pressure surrounding the blood vessel The pressure gradient across the vessel wall is called transmural pressure" It is defined as the difference between the intra vascular and extravascular pressure In its recent use, the term effective pres sure appears to be synoaymous with transmural pressure For complete analy of a system with flowing blood one must consider the transmural pressures in addition to the pressure gradient along the flow paths ·III Factors Affecting Venous Return This chapter is confined to a brief resses of those mechanisms which alter and shift the volume of blood contained in the senous system Here as later at appears desirable to consider the pulmonary circut as part of the senous sys tem since some factors which affect venous return to the right heart also affect return flow from the pulmonary veins to the left heart In general the changes brought about by shifts in blood volume are relatively slow as compared to the more dynamic effects caused by the action of the heart respiration and skeletal muscles The rapid dynamic changes will be taken up in Inter chapters Since the return fios of blood is an integral part of the entire circulation at caunot be considered in an isolated manner This holistic aspect is emphasized by the observation that the same factors (1 2somotor activity granty etc) which affect venous return also influence the artersal side of the circulation However there is a quantitatre difference insofar as one side of the circulation is more affected than the other The difference in structure bettseen the renous and arterial system is mainly responsible for this the enous walls being thin and collapsible whereas the arterial walls are thic, and relatively rigid EFFECT OF GRAVITY ON VOUS RETTRX The unique features of the circulation in the veins are to a great extent due to the wall structure which permits nenous filling to fluctuate within a wide range without an appreciable change in transmural pressure Veins are rarely fully filled and distended Thus the venous system can accomodate widely vary Rg volumes of blood This phenomenon accounts mainly for the effect which gravity has on venous return If veins and arteries were rigid tubes flow in theou mould not be affected by a positional change Floty through such a rigid ay stem would only depend on the arterior enous pressure difference at heart level other factors remaining con stant This situation is symbolized in Figure 3A If a rigid V tube tinch had been previously in a horizontal position were suddenly tilted into a vertical position the same amount of blood would return on the venous side which was put into the system on the arterial side However this is not the case in a distensible system Oning to the relatii els greater filling capacity the venous side in the body is much more affected than the arterial esde by a change from the recumbent to the erect position as illustrated in Agure 3B In normal man the reduction of venous return under such conditions is usually of brief duration because a number of compensatory vasomotor mechanisms come quichly into play Hossever it is doubtful that even with the aid of these mechanisms the same amount of blood is returned to the heart of man in the erect as in the recumbent position If venous return and subsequently cardiac output are greatly reduced orthostatic famtibg interyenes As is well known the compensatory mechanisms are diminished or become snadequate after long bed rest and so a number of diseases 15 ·16 EVOUS RETUR: Figure 3B also helps to explain the basic mechanisms by thich baths hasc a bencficial effect upon icnous return in certam circulatory disorders Immersion of the body below heart level reduces the pooling of blood in the dependent parts by increasing intru ascular pressure and makes available, at least tem poranly, 1 greater amount of blood to the heart for cjection (For discussion see Gruer 1955b) Animals which usually do not assume an upright position have less efficient vasomotor responses than man They are almost noneustent in the cel and snale, which can be killed by immobilization in the vertical head up posture These animnis "bled theinselves to death" into their venous system (For lustory and details ce Franl lin 1937) If in normal man the force of gravity in the licad to foot direction (positie acceleration) is increased beyond a certain degree and duration, venous return becomes so greatly reduced that sincope ensues (blackout" of pilots) This is symbolized in figure 3C In this example it is assumed that 10 times the normal gravity (10g) will distend the veins to such a degree that they accommodate 1 very large portion of the blood volume and that actie vasomotor mechanisms are not strong enough to counterrct the presive force of increased hydrostatic pressure As a result practically no blood rctuins to the heart The arteries in the dependent part of the body would also distend but not nearly to the same extent as the veins On the other hand if 10g act on a rigid U tube, flow throull it would not be altered (Fig 34) Comparison of the diagrams 3A and 3C also illustrates the basic mechanısın by which a pressure suit may hue a beneficial effect on scnous return in pilots The suit > pressure on the walls of the entire scnous system below heart level counteracts the extreme distension and presents to some degree the pooling of blood The pressure suit is meant to convert the distensible system shown in Fig RETURN ZERO HEART LEVEL RIGID ARTERIO VENOUS ARTERIOVENOUS U TUBE SYSTEM SYSTEM allgor 10g at lg of 10g *I( LRF 3 Iffet of normal and increased gravits on the distensibilits of the scnoue estem Ivanatın in text ·FACTORS AFFECTIVG VENOUS RETURN 17 FIGLEE 4 Influence of centrifugal force on vedous return in a monkey Left \ormal gravity Right 6 times normal gravity head to leg Blool contains thorotrast Both pictures taken in diastole animal sitting brared and additionalls supported by a collar around the nech Centrifugal force loforms thorus and lepres.cs daphr gm (From an Iran einemato grar hic film, Otto H Gauer) 3C into one which approximates more closely to the rigid system shon n in Fig 3A The effcct of increased gravity on senous return is illustrated by two pictures elected from an x ray cinematographic film taken by Gauer (1914 1930) on a centrifuge (Fig 4) In the photograph on the left a ray opaque material enables one to discern the size of the normal heart and great ses els and the density of the well perfused lungs On the right side at 6g the size of the heart and great Vessels is drastically reduced The lung fields are almost clear indicating that only little blood perfu es the lungs The pulmonary vascular tree is outlined be low but not above heart level demonstrating that cien nithin the pulmonary circuit the return flow of blood is grcatly interfered with (For details concern ing the effect of normal and increased gravity on venous return and the activity of compensatory mechani ms consult Fulton 1948 Landis 1948 Gauer 1950 1955 ) Upon assuming the creet position the veins in the dependent parts increase in fullne s by the force of gravity whereas veins from the upper part of the body are emptied toward the heart These upper reins collapse partially upon depicting their content and their intravascular pressure approaches zero Values less than zero are presented from occurring by this collapse In spite of a partial collapse of the veins above and distension of those below heart level there exists a favorablc pressure gradient for venous return from all peripheral regions to ·18 VEVOUS RETURY the heart (Fig 5) In order to illustrate the principle of the mean flow gradient, venous pressures in the upper and lower part of the body are indicated without regard to venous valves and negatne intrathoracic pressure Intravascular venous pressures are measured against atmospheric pressure Above heart level the venous pressure is practically zero duc to partial venous collapse The pressure gradient along the venous channels is the height of the hydrostatic column above heart level The gradient is great but resistance to flow in the partially collapsed veins is high (see also Chapter 6) At heart level 17 "0" ne baretowe LE TRAITS TAURORLUNNI FI LREJ Simplified schematic diagram of scaous intravascular pressures at different points above and below heart level in inan iilu trating the ar tual pressure gradicats available for the return flow of blood along the senous vascular bc 1 Description in text (Modified after figurcs 1 an 1 3 of Duomarco and Rimını 19 01) ·TACTORS AFFECTING VOUS RETURN 19 (phlebostatic level) venous pressure in the right atrium is assumed to be close to zero Below heart level the venous pressure gradrent responsible for blood flow from the periphery toward the heart is the measured z enous pressure minus the hydrostatic pressure column This gradient is small as indicated in figure 5 by a dotted slope but resistance to flow in the distended veins is very low Flow from the loner extremities to the heart does not have to overcome a resistance of the hydrostatic pressure column as is occasionally believed The hydrostatic fluid column is the venous limb of the U shaped arteriovenous communicating tube system which as such does not hinder flon (Fig 3) The hydraulic pressure gradients and their probable effect on venous return have been the subject of numerous studies by Duomarco and his co workers from 1944 to 1954 It should be pointed out however that the determination of pressure gradients alone without accompanying fox measurements does not provide accurate information about venous return It must be borne in mind that the force of gravity does not accomplish work over a period of time just as static negative intrathoracic pressure due to lung elasticity is not performing work (see page 7) Only a change in gravity or intrathoracic pressure does work which can alter bloodflow Summarı ing In an upright position gravity shifts blood into the vessels of the dependent parts of the body A larger amount is accommodated in the distensible veins than in the more rigid arteries Venous return is thereby reduced if compensatory mechanisms are inadequate Above heart level the veins are partially collapsed and the pressure gradient for flow along the venous channels is given by the height of the hydrostatic column abose heart level Below heart level the veins are distended and the pressurc gradient for flow along the venous bed 18 given by the enous pressure minus the hydrostatic column VENOUS VALVES If the amount of blood available for filling the reins were not limited the presence of venous valves would not be necessary for the movement of blood from the dependent parts of the body to the heart, because teins and arteries are a communicating U shaped tube system (Figs 3 and 5) The essential function of the venous valves is to break up the high hydrostatic fluid column into sinall segments so that tiie venous reservoir is not overfilled by the full pressure of the uninterrupted column In Fig 64 the venous pressures in two segments of a vertical leg vein are shown during the condition of muscle relaxation The pressure in each segment is the short hydrostatic column of 100 mm of water plus intravascular pressure which additionally distends the vessel wall (90 and 80 mm of water respectively) Flow from the lower to the higher segment does not occur under this condition When the lower venous segment is locally compressed eg by a muscle con traction exerting a pressure of 100 mm of water on the outside of the venous wall pressure in this segment briefly rises above that in the higher segment and flow is established (Fig 6B) The breaking up of the hydrostatie fluid column into small segments pre ·20 ENOUS RETURN 80 90 les 100 100 MUSCLE RELAXED MUSCLE CONTRACTED FIGURE 6 Pressures in segments of a vulved vein illustrating the interrelation of hudo static presure and lateral pressure at rest (muscle relaxed) and during a localize I mu clo contraction Pressures in mm of water Length of each venous segment betueen tuo valves 100 mm Description in text vents the on crdistension of the thin cnous walls which would occur under the continuous weight of the entire fluid column During movements relatively small lateral pressures on the outside of the venous walls are sufficient to overcome the mall hydrostatic pressure of short Vertical segments of the venous blood column When valves are incompetent a high fluid column overdistends the veins and due to a high pressure (= filtra tion) gradient across the venous and capillary walls orthostatic edema may ensue (For dctuls of valic structure and action sce Franklin 1937 Burch 1930 ) Through valvular incompetance the short hydrostatic pressure columns of scy cral segments may be joined to form a high fluid column The continuous dutension of the scnous walls by a high fluid column may lead to the formation of varicoce cins (see Harri on 1994 Montgomery and Zintel 1934) Dc pite a larger accomodation of blood in the varicose veins total venous return would not be reduced after the initial filling of these varicose rescrvoirs has been ac complı hed The phs iologically indicated treatment to counteract the con tinuous venous wall oi erdistension appears to be an intermittent reduction of the hydrostatic column (og by leg clevations) an increa c of extrala cular counterpressure (eg by clistic bandages) and a surgical con-truction of now venous vales (Ei emin and Valette 1953) Summan ang Venous vals es break up the lugh hydrostatic fiuid column into sinall segments and present oserdi tension of the thin wallcd cins in thic dependent parts of thie bowls ·1 *CTORS AFFECTIVG JENOS RFTURY 21 TEVOLS DISTEISIBILITI AND TOVE As mentioned above a number of reactions come into play when a person assumes erect posture The responses by which seins and small vessels may counteract distending forces and thus prevent exces ne pooling of blood have becn of greatest interest to physiologi ts and chimcians (for reviews see Franklin 1937 Burton, 1954 Folhos 1935) Though not well documented, many of these reactions have been postulated and described previously in textbooks However only recently have animal experiments under strictly controlled con ditions established conclusive cvidence for the eustence of specific reactions of the veins in the regulation of the circulation When the volume of blood in a normal partially collapsed vein is suddenly augmented the intravascular pre sure barely increases until the vein becomes round and reaches a certain degree of fullness The volume increase up to this point corresponds to the filling of a collapsible bag or tube without distending the walls True disten ion of a vein occurs only when further volume increments lead to an clevation of the intravascular pressure Contrary to common belief inost exciscd veins are little distensible in the transier e direction though more casily stretched in longitudinal direction It appears that in the intact organism cins al o have a low distensibility upon sudden volume increase (Alexander 1948b) The initial low di tensibility undergoes a change however if the in crea ed voluine remains in the venous bed for a longer period Under this con dition the scnous walls give' slowly This phenomenon which has been called stress relaxation or delayed compliance has been demonstrated in the portal system by Alexander et al (1953) and in the pulmonary system by Sarnoff and Berglund (1952) It is attributed to the visco elastic properties of the smooth mu culature in the vessel wall Whercas the low distensibility of veins may counteract sudden transient pressure increases and thereby avoid pool ing of blood sustained high scnous pressure may result in significant pooling due to the delayed compliance of the venous walls An important factor which counteracts venous distension is the contraction of smooth muscles in the walls of the veins by adrenergic stimulation Since active constuction reduces the radius of the vessel the effectiveness with which the wall is capable of resisting distension is greatly enhanced (effect of Laplace) Such va oconstriction would serve to mobilize blood for return to the heart Since venoconstriction can be elicited by the same reflexes which are known to raise arterial blood pressure (pressure reflexes) the venomotor activity appears to be an important contribution to circulatory homeostasis just as are the well known adjustments of cardiac output and arteriolar resistance (Alexander 1951a b) During irrever ible hemorrhagic shock the ychomotor mechanism fails this leads to a marhed pooling of blood in the venous system (Alexander 1953) Summari ing Veins have a relatively low distensibility upon transient increases in intra Vascular pressure Their smooth muscles contract actively upon adrenergic and reflex stimulation and contribute siderably to circulatory adjustments Pool ing of blood in the splanchnic venous system occurs due to på sue yielding of ·22 VE VOUS RETURV the venous walls upon prolonged action of intravascular pres urcs, phy svological reflex Veno dilation and failure of the renomotor mechanism in irrei crsible hemorrhagic shock VERIOUS AVD HUVORAL REGĻLATION Undoubtedly the specific refies venomotor activity of the splanchnic bed dis cussed above is a factor of fundamental importance in the nervous regulation of venous return Apparently the same adrenergic reflexes which evol e splanchnic venoconstriction bring about arteriolar constriction in the entire organısın and by & simultaneous generalized venoconstriction cause a transient increase in total systemic venous return (Rashl ind et al 1953) On the other hand, cholinergic reficxcs which lead to arteriolar dilatation also dulate the rems and result in a temporary decrease of total venous return by blood pooling in thic Venous channels The profound effect of adrenergic and cholinergic stimulation upon the voluwc elasticity characteristics of the venous system is graphically illustrated in Fle 7 These characteristics have been assessed by Peterson (1951, 1952) through rapid short duration fluid injections into the abdominal inferior caval trec of dogs The modulus of distensibility of the veins is plotted on the ordinate again t the intravenous pressure (abscissa) Curve A shows that under normal conditions the veins are not completely filled The sharp break in the curve at a pressure of 100 mm of water indicates the point at which the vessels become round Then up to about 270 nm water the curve remains flat indicating that AP/AV is constant Above this pressure the curve rises and becomes nonlinear presumably because of the distensibility characteristic of muscle and collagenous tissues in the venous walls Curic B indicates that cholinergic stimulation leads to a marhed venodilatation (brcih in curve at 180 mm water) which would permit considerable pooling Following the injection of epinephrine the veins become round at a pressure of 40 mm water This fact and the stocp slope of the curve indicates that the veins are more rigid and contracted during adrenergic stimulation (Peterson 1956) The entire venous bed may therefore be looked upon as a variable blood depot Blood in this type of a depot is honeser, not withdrawn from the active circulation It merely circulates slouly when the venous channels are widencd by prevailing parasympathetic tonus Since the central veins constitute a con siderable part of this depot,' blood is readily available for a sudden increase in right heart inflow and subsequent output as demand arises A corresponding condition prevails for the left side of the heart as pointed out by Sjostrand (1953) Here the pulmonary vascular bed represents a readily available large re crvoir which permits a sudden increase of left heart filling and output Thus Tould serve specifically for the rapid adaptation of the circulation to positional changes and physical work The dynamic mechanisms by which the action of the heart can contribute to its filling from the reservoirs will be taken up in chapter 9 The importance of the large pulmonary blood depot which 19 immediately arulable to the left heart and systemic arteries hould be emphasized Iccord ing to Sjöstrand (1993) about 30 per cent of circulating blood volume is con ·FACTORS AFFECTING ENOUS RETURN 23 20 EPINEPHRINE AP AV 15 10 (A) NORMAL 5 в) VAGAL STIM 100 200 300 400 MM H2O FIGURE 7 Volume disten ibility haracteristics of the venous system under (1) normal con ditions during (B) cholinergic and (C) adrenergic stimulation Ordinate 1P/AT 12 mm H O/Ml volume change Absc15.2 mm water pressure measured in the inferior vena casa 1 tal to the renal seins The values are limited to pressures occurring within the phy 810 logical range in the venous stem (Modified from unpuble hed data after Lysle Peter on ) tained in the thorax of the normal human in the recumbent position Three fourths of this amount is in the pulmonary Vessels and one fourth in the heart during dia-tole The volume of reserve blood in lungs and heart is larger when vagotonus prevails and maller when sy mputheticotonus prevails Trained athletes have a greater blood volume than average persons and their thoracic blood reservoir is accordingly larger Since this reservoir is propor tionally distributed betn een lungs and heart their residual ventricular volume at rest is larger than that of averige ubjects (Reindell et al 1933 Gauer 1955a) Upon sudden demand by phy sucal exercise the large residual sentricular sol ume and pulmonars blood re ervoir tre first called upon to pay for the deficit between the temporaril laging systemic venous return and the immediately increased left ventricular output This period of dynamie imbalance lasts only a few seconds until increi ed return from the s} temic reins due to reflex Venomotor action (Page et il 1938) oecurs and as a con equence of increased ·24 TE VOLS RETUR left heart output restores the equilibrium at a higher level of flow A correspond ing situation prevails when a person rises from the recumbent position As men tioned before return from the systemic veins is then briefly reduced (Fig 3B) In normal man approximately 600 ce of blood suddenly sags into the vessels of the dependent parts Thus amount is immediately compensated for primarily from the intrathoracic blood depot It is important that a large intrathoracic reservoir is available for left heart venous return to prevent a temporary re duction of left hicart output which may lead to a drop in arterial blood pressure and subsequent orthostatic fainting Truined athletes have in these re pects better than normal compensatory abilities owing to their relatively larger tho racic blood depot If the intrathoracic blood rescrvoir is diminished from 30 per cent to less than lo per cent of the total blood volume then this reservoir becomes inadequate and left heart output decreases temporarily upon postural changes Under these circumstances the left heart cardne output depends directly upon the fluctus tions of the return flon from the systemic cins (Sjostrand 1953) Anesthesia surgical trauma and open thoracotomy luft the blood in the organism in such direction that less than 15 per cent of the total blood volume is contained in the thora. This explains why aside from other factors under thcsc conditions the latitude of circulatory regulations is greatly diminished It explains also how in experiments on anesthetized animals the importance of the thoracic blood reservoir for certain sudden circulatory adjustments has not been fully appre ciated This has also been pointed out by Rushmer (1954, 1955a) Apparently the basic relations of venous return and cardiac output as represented by Star lungs law can be ou crshadowed under normal physiological conditions by the mechanisins outlined above but they come into play when the circulatory is dmn lcd and under pathological conditions The well known blood depots in spleen ind other organs seem to have the role of auxiliary depots which are called upon if the readily available blood reservoirs in the lungs and systemic veins (ind po sibly al o portal seins) are insufficient to meet the de mands (For revicus on blood depots prescor reflcxcs and humoral control con sult ligger 1990 Fulton 1935 Hous 1 1930 Rodbard and Katz 1935 ) The regulation of venous return and blood volume distribution is arded by ? number of reflexes which are elicited from stretch receptors in thic venous walls though difficulties have been encountered in establishing clear cut evidence for the cistence of some of the e rcflcacs (reviched by Ivado and Schmidt 1930) Drutension of the car il cins and right atrium rcduces reflexcly the tone of the vigus nere and accelerates tlic licart (Bainbridge reflex) A similar reflex is chic ited lyx pulmon in venous dilation (Talino 1931) Risc of pri ure in the ab clominal casal tem initiates 1 icno venous reflcs by aluch the sympathetic ton of the inte tinal veins is reduced (Alexander 1906) In addition to those circulatory dynamic effects the timulation of stretch receptors in the area of the breat veins heirt and pulmonary ve els enhances urinc flou These receptors appear to play an important role in the control of plasma yolume and central Venous pres ure (Gruer ct al 194 Henry Gauer and Ruus 196 lenty Cuer und Sicher 19,6 Gauer et al 1936) Locul di ten ion of the walls in peripher il cina re ults in con triction of the 10 crie ·F1C1ORS AFHI CTIVO IF YOU RETLRY 2 arteriolus supplying the particular venous bed Thic throttling of artcriolar in flou diminislics in turn the cous engorgement (negatiic fudback ) Tlie precise nature of this seal vasomotor rcflex remuns to be clucidatud espe cially whether or not it is a truc reflex uxon reflca or other mechanism (lamada and Burton 1914 laddy and Gilbert 1976) Summur ing The entire venous system becomes dilatul but loss distensible upon choliner gic stunultion whereas it is constricted but clastically mort distensible under Idi nergie influence Central systemic ruins and the pulmonary vascular bed represent variablc blood depots wluch are ie wlily an ulable for increase in heart inflow and output upon sudden dem inil In normal recumbent man the lirge blood rescrvoir in lung and leart is imıncdiatiks utilized durin, sudden physical work or positional chantc to increase left stroke volume before systemic venous return can be inci cand appreciably When the thoracic blood rt croir is reducid in ancsthesii or by truuma the output of the left heart depends directly upon fluctuations of yutumnc venous return Reflecy from stretch receptors in the cnous » ulls nav aid in regulating lıcırt output the total circulatory fluid sol ume and arterial inflos into local venous beds ·IV Present Problems of Venous Return Dynamics From the historical rovicus in the first chapter it is crident that our knowledge of the forces which determine the return flow of blood needs further expansion The present basic problems concerning the dynamic aspects of venous return can be crystallized around the following three main topics (1) The effect of venous collapse on pre cure and flow in the veins (venous liemodynanıcs) (2) The effect of respiration on 1 enous return and (3) The effect of the heart s action on nous return EVOUS COLLAPSE PHENOVEVA The concept of Holt (1940 1941 1943), that venous collapse can 1cduce blood Hon through a vein despite an increase in the pressure gradient along the vessel has strmulated the investigation of hemodynamics in the venous system It 18 well known that in the hugh pressure system of the arteries volume flow through 11e se increases with an increase of the pressure gradient between an upstrcim and downstream point of the vc acl if arteriolar resistance remains unchanged Therefore pressure measurements at different points along an artery permit a fur estimate of quantitatic changes in volume flow Thus situation prevails becausc arterics with semi rigid elastically distens ble walls behave e sentrally like uniformnly patent tubes Tlus is not necessarily no on the verous side In a los pressure system with collapsible tubes the pres sure gradient between two points may not give information about the volume of blood flow between the points for caample pressure at a distal point of a vein may be 0 nin water and at a piouimal point 10 mm water but volume flow through the vessel may be practically nonexistent because betucen the two points a segment of the ses el may be partially collapsed causing a high resist ince Therefore in this cic measurements of senous pressures cinnot give in formation about changes of blood flow through the veins A well known e ample from the studcat laboratory illustrates (luis situation \ cnous pres. urc falls slightly in normal inspiration shen it is measured directly with the Voritz and Tabora inethod in the forcırm During in piration the pre sure gradient between the forearm and right atrium increases and one might conclude that an increased amount of blood flous from the foreirin to the heart During deep in piration scnous pre sure in the forearm rises slightly Tlu pro ure difference betucen forearm and right atrium has become considerably fruiter with deeper in piration avertheless nc shall di cu sin detail volume llow does not nece arily inerea e Thc pre ant problemi therefore to study in the venous system the pressure flow relation which are to a great extent determined by the collap iblity of the Un 70 ·IRLSEVT PROBLEMS OF SEVOL RETUR DILNICS 27 CO TROVERSIAL EFFECT OF RESPIRATION Clo ely linhed with the first topic is the intriguing controversy as to whether or not venous return is aided by respiration As already mentioned there are two diametrically opposed schools of thought One repre ented by the clasical the ory of Donders is based on the assumption that cins behave like arteries as uniformly patent tubes Flon in them would increase directly with an increase of the pressure radient If for example the pressure gradient between the jugular vein and the right atrium is increased by inspection inflok into the right heart would be augmented the other view the collap e theory states that except for abnormal and pathological conditions the negative pressure in the thorax and ats variations are incapable of influencing venous return directly (Duo marco Recarte and Pimini 1944) A reinterpretation of the known data could never reconcile the two conflicting VICW It has been necessary to dev clop new experimental approaches to resolve the problem THE HEART AS A FACTOR IN ENOLS RETURN The last problem wluch still calls for elucidation after centuries of controversy is the que tion Docs the heart by its own action draw blood toward it or not? Is it a suction pressure pump or is it a pressure pump only? This problem pre ints two facets First what is the effect of ventricular sy stole on venous rcturn and second what effcct has ventricular diastole on venous return? Bohme (1936) belici ed that he had solved the fir t problem by the use of x ray-opaque material in the veins His observations are adequate evidence that the ventricular contraction can accelerate blood flow in the thoracic caval vein. However this acceleration of the blood column does not mean that rikt atrial inflow 1e quantitatrely inerea ed during sy stole by myocardial contrac tion Bolimes findings are purely of qualitative nature as pointed out by Holzlohner and Schoner-tedt (1940) Bolime himself stated repeatedly that during the period of sy tolic acceleration of blood flow both caval seins nar rond Thu indicates that the amount of blood passing quickly through the veins durin, ventricular systole could have been cqual to or cien less than that flowing during diastole Actually in a vein one cannot predict from an accel eration of flow whether more or less blood passes through the vc sel because thic cro sectional area of a vein varies remarhably For example The shape of the central veins could be nearly circular during sentricular diastole and a large volume of blood might fion slowly through the wide open vessels into the heart On the other hand the veins may become elliptic due to the partial collap ( during sentricular systole and only a small volume of blood might pass through the nirron cd vessel into the right atrium though it would flon at a lugh rate The present techniques of x ray cinematography cannot provide a quantitative re olution of this problem Another difficulty of Bohms method should be pointed out He could only ob crie an acceleration of the blood column during y stole and deceleration during dia tole but details of the time coure of the events could not be es ·28 SEVOL RETURN tablished by hut Holzlohnci and Schoner-tedt (1940) found that volume flow in the external jugul ir vein of the do, durin, Icntricular sy told u is not nearly so breat as inticipated or suggested by Bohme s qualitatic observations How ever Holzlohncrs data do not resolve the problem either becluse he undertook the flow measurinents in peripheral van where arterial impact and various unanalyzed artifacts app sentis di torted dus curits He could not coritate accurately the flow changes with the cardımc cycle and did not record pe ures simultaneously A nes quantitatic approach is theicfort nece try to study the force which the ventricular my ocirdiac contraction may cacrt on venous return The second facet of the questionable suction pressure pump action of thic heart deals with the cffect of ventriculu dia tolt on scnous return At pie ent, these is no conclusive experimental evidence 11 ailable to invalidate the dictum of Wiggers and Struub w duch states that di istolic ventricular inflow must be passic Incc no negative pre sur las been recorded relibly in the sentricular cavity during diastoli (For 1 discussion of the carb) avulable for a spad di tolic filling «ce also Rushmer et al 1933 ) Thus it is up to the proponents of the oppo ite vu (Guap 1934 Cignoliny 1951 Villa 1941 to furnish indi putabli capement il evidence that blood is actively suckal into the ventricle at the beginning of diastolo (scc al o foot noto page 110) The e basic problems we internoicn with the brouer pects of venous return which rulate it to liomco tatie mechaninis (I und 1900) wd to tlıc ret of the circulation in hicalth ind di cise Grun (1948) summarizu thic integration of the different problems ind the difficulty of r olving the by the use of pressure ineasurements is follow Recent interest has been focu ed on the mechanisms controlling venous icturn both under play jologic conditions und in dı-turlances of liomcosta 15 such as the con un lock and heart fuluc Attempts in this direction have been made by accordin, imultaneously the right atrial pro surc cudnie output and sortic pre uit Honcier, intepreta tions of the data ire complicated by fluctuations of central venous que surt produced by ri piration by the fact that extremely large 1211 itions in the quintity of blood in the central rains and trı: may occur with little chingc in loud of the recordel pie suri înd finally by the fact that cardiac output muy vary independently of the central venous reservoir pressure and therefore re ult in change of atrial ple mult in a direction oppo ite that capected to result from the simultaneously occurring variation in schous return Fluctuations in capacity of the central venous reservoir ind atrium may also causc 1 chinge in level of pre ure in the e structures in thic ib cncc of any alteration in cudic output or venous return thius furtlicr complicating interprctation' From the foregoing it 18 cuident that descriptise ob crvation and circum stuntial cuidence from pre urc mchurements Bluch lind it elf to various interpretation cannot penetrate to the core of the problen In this field is in miny others in modern biological ciences the older techniques of a dc criptae ind ob erving approach mu t be repliced or at ict supplemented by qu in titative methods In recent yenrs the most fruitful approach has const ted of measuring blood ·TRET I ROBLEX OF YEYOL AFTLA DIVIN 99 cec jou directly and quantitatiicly in the sebous system and correlatn, it with the smultaneously Tucorded pressures in the ve els In order to gain quantitative information of hemodynamic events it is ale aj s in to measure tso parameters Ļ& fox and pressure gradient along the cuter ved for determining the third resistance (Q = P/R Chapter 2) Measurements oí pre ure alone can furnı h only indicative endence Tech pically it is much ca ier to mnc i ure pre sure than flow Jarsch realized this dilemma as early as 1928 nhen he stated for the duvelopment of circulation recerrch it has certainls been a disaster that it is relatnch cumbersome to determinc volume flom but so<?) to measure the blood pres ure For thus rer on the blood wie manometer has gained a rather fascinating influence though mo t organs do not nied pressure but plume flon Althou Jarsch bad primarily arterial flox in mind bis statement is een more applicable to the vious ystein For technical reson measurements of blood flow in the los pie sure system of us >> much more thifficult than in the high pres ure system of the arteries Grcat efforts are therefore been made in recent years to dar clop venous blood flow recorders Gee much of the succes in approaching pre ent and future problems depends upon proper instrumentation the neat chapter is devoted to a detailed surse of techniques of blood flar recording Summan ng Three basic problems of venous return tale the center of scientific interc t at present Thesc arc (1) the effect of venous collapse on Yussure fon relations and scnou bemody mcs (2) the influence of re piration on venous return and (3) the attraction of blood in the sessis by the hearts our actron during systole and/or diastole An elucidation of the e problems depend a great deal upon direct and quantitatne measurement of senous blood Ron ·V Methods for Venous Flow Measurement In the search for the ideal flow meter scientists have developed instruments wluch make use of almost excry concen able physical principle Each instrument has only a limited application, and numerous disadvantages There is no um versal flow meter which is preferable to all others The choice of the proper flow meter depends upon the nature of the problem in whose solution it is to be cmployed Generally speaking the simplest and most direct method is best Considerations here are restricted to the specific aspects of venous flow apprratus and their recent des clopment For an account of flow meters in general the reader is referred to the cxcellent articles of Green (1948) and the new (lighth) voluinc of Vethods in Vedical Rescurch For an understanding of many flon tracings shown in thus booh, the difference betwcen two types of continuous flou recording should be mentioned The two types are cumulative recording and rate recording 1 Cumulative (also called slope or integrated) recording is most advan tagcou ly used to mea urc venous drainage, though it can al o be used for flow meters inserted into a vcsacl Flou is recorded as a slope (Figs 24 and 28) The higher the flow rate the sticper the slopa A con tant flow rate produces traight sloping line (Fig 24B) change in flos rate produces a chinge in the angle of the slope Before flow begins and again after it ends the tricing forms a horizontal line but the two are at different levels Volume as messuicd by the difference in level it the height of the tracing The advantage of cumulative flow recording is that the total volume during a given time interval ini be measured directly on the record It is not necessary to integrate different rates of rapidly changing flow in order to obtun total flow 2 Rate (also called s clocity | recording is more frequently used to nic isung uninterrupted flow through 1 ves cl The flou rate is recorded is an clevation of thie tracing above the zero line (Fig 30) I constant flow rate produces ? horizontal linc Increa c in flow rate leads to an upstroke decrease to a down trohe of the curve In the absence of flou ( zero flon ) the tracing returns to the zero line The volume is calculated by measuring the arc, under the flon curse Two types of direct flow meters have been successfully employed for a study of icnous flow dynamic The e dre (1) Venous drainage flow meters and (2) Pul atile flow meters TEVOL DRAIVAGE RECORDERS Tlus method 14 tlic implest Outflow from a cannulato sun is collected ind continually registered Vot devices used for this purpo c irc cumbersome und have such breat inertia or friction that they cannot faithfully follos rapid flos chinges (Brubach 1947 Ligon 1917 I indgren and Linus 1994) The bit in truments ir thic train giuge flow meter of lica inder (1918b) the tambour ·VETIIODS FOR EVOLILON WEAL REVET 32 0 P T SC FACE ** & Salemate diagram of an optrcalls reconling Tambour flowmeter Description in text fouincter (Brecher und Ritter 1951) and the mecbanical balance of Zacche ct al (1955) The first mentioned has the advantage of greatest flexibility and casily adjustable sensitnitz As the tambour flow meter was used for sencral studies reported here it is described briefly (Fig 8) Blood from the cannula I drains into a secener o Its acigit presses on & tambour 1 which transmits the pressure to an optual minometer G by a liquid system & light beato deflected by the mirror on the manometer makes sloped tracing on .s photokymograph The natural frequency of a fouincter system of 20 c3 cles, see pærraits tracing af sudden fon rate change nith a minimal time lag The calibration reserlo ? linear response of the instrument Summon ing Inous drainage recorders of adequate frequency response can be sutable for nesurement of moderately fast changes of thous for They are not ndiquate for recording variations aier singic cardiac cycles RECORDING OF PULSATILE FLOW For better under tundin, of pulsatile fion meters brief mentson hould be made of mean flow recorders some of which have also been employed in the \CDOUR system Vean recorders can only register the moun or aterage rate of flou Cau cs for the inabilty to follos quich chati ca of fion include mechanical ·32 VE. VOUS RETUR inertia damping friction the length of time necessary for observing the more ment of the blood, the slow frequency reponse of electrical amplifiers or a combination of any of these factors Attempts have been made to record pulsa tile changes in veins and artcrics with mean flow recordera The cumulative curse which Burton Opitz (1902) trued with a modificd Hurthic Stromuhr in the cxternal jugular vein of a dog may serve as an cxample (Fig 9, left side) The middle record of the thrce shows by the steeper slope ( 4 B and CD) an incrcase in blood clocity The e curses hare often been reproduced in tout books as cridence that nous blood is suched into the right atrium during ventricular sy tole (4B) However it should be pointed out that this cudence is of a qualitative nature only Tlie Stromuhr (Fig 9 right side) has too much inertia to permut a faithful reproduction of flor cients Thc moving parts overshoot greatly once they are act into motion Straub (1923) and Holz lohner and Schoner tedt (1940) called particular attention to the fact The estimate of Bolime (1936) that ten times as much blood flous toward the cart during ventricular systole than during diastole was mainly based on the quan titatively incorrect figures of Burton Opitz (1902) It mu t be realized that the same physical criteria which Otto Franh dc inanded for accurate minometry also apply to phasic flon recording In order to obtain a faithful reproduction of rapid flon changes the recording instrument mu t have a high natural frequency reponse just like a manometer However it is casier to meet this standard with a manometer than with a floxacter and easier with flow meters used in the arterial system than with tho cu cd in the venous y tein In arteries it doce not inatter much if a flow meter introduces a inoderate re i tance to flow becau e the pressure in this system is high and some pres ure lo s can be tolerated For example a pressure drop of 5 nim Hg across 3 flor meter will not interfere greatly with the circulation of the pressure head available is thereby reduced from 120 to Ilə mm Hg On the other hand an equivalent resı tance introduced into a vein would lead to congestion di tal to the flow meter becausc scnous and capillary walls yield more than anternal walls When Smith and his co workers (1932) in crted a rotamcter into the central venous circulation of dogs this re ulted in a rapid circulatory collap c since the animals were unable to raise i cnous pressure to and maintain it at a levcl high enough to overcome the re i tance offered by the rotameter The problem of an undul great re istance introduced by a flow meter par ticularly concerns the ve of the differential pre sure flow meters These in struments have a lugh natural frequency re pon cu hich makes them suitable for pharc flon recording Hon(er in order to obtain adequate sensitivity appre ciable re i tance mu t be introduced into the ves el Thic problein of de igui in a differential pre ure formeter is to find a compromi e among rc i tance ensitivity and frequency re pon e For quantitative mea urement of flou hy mctors that record vclocity and direction at 19 indı penable to hnow at each moment the cro s sectional arca of these d through such the fluid volume pas (9 is pointed out prcyzou is in the di cu jon of the rav ob criations of Bulime 1 vclocity increase of the fluid colunun doc not nece arily incan that the volume of fluid is incrca ing ·NEG PR IN PL CAVITY 15 sec BLOOD FLOW EF GA B D O GAB O VIETITODS FOR JE VOUS FLOW MEASUREVETT B C E F GA B VENOUS PULSE B Tht cardiac variations FICURD 9 Flos truung obtained from the external jugulur vein (EJ) with a modified Huthle Stromulir (right) by Burton Opitz in 190 They llu trate how artracte created Lth incrta of a low frequency recording tem can distort flou curve Synbols of tracings to the left (approximately iclated to cudic cycle) C = beginning of atıl Jatole A = peak of atrial s stole B = earls ventri ulur cjection C= end of ventucular ejection D = 11pul ventricul ir inflor The L = low ventricular inflow me I = di tasi Simbols of Stromuhr to the right lind B = cannulae in jugulu ycin C = cylınırr filling watis bloo l enteuing at L ind leaving nt T I = plunger moyed by blood T = trans mion to lover LD = plate which cmt rotation of Stromuhr for filling the cylinder in reicie direction after plunger has moved up Cannulae connection, after turning of D ac indicated to dotte 1 lincs ·34 VE VOLS RETURN proportionally Unrecorded fluctuations in the diameter of the scsscl preclude any measurement of volume flow This factor is of greater importance in ruins than in arteries since the cross sectional area of veins usually undergoes greater fluctuations than that of the arteries Vomentary area changes in eins are caused by collapse whereas in arteries they are caused primarily by clastic e pansion Two procedures appear most fruitful in establishing quantitatively reliable conditions for flow measurements in veins These are (1) continuous recording of the normal fluctuations of the cross sectional arta or (2) fixing the cross sectional area of the vessel at the point of flon nicasurement The latter m13 be accomplished by inserting a ringlihe structure (Fig 15) or by expanding the vessel from the inside or outside by mechanical means (Fig 17) In arteries tlus problem is casier to solve because their expansion can be prevented by applying a ring or slccre around the vessel as commonly done in the use of electromagnetic flow meters Distortion of the flow pattern may also arise from the use of overly long tubing to conduct blood to and from the flow meter Long tubing may delay the flox pulso though tlus effect will be of little importance of the tubing is rigid and not excessively long Further the fluid column in 1 rigid tube may through its inertia cause an overshoot of the column upon rapid acceleration or deceleration This can be corrected by judicious dampin, cg, with a scie clamp However since damping increases the resistance to flow, this procedure can only be used in the lugh pressure system of the arteries If the wall friction of the tubing is too lugh the full extent of the flow accelera trons and decelerations can not be recorded the effect would be the same as overdamping rigid tube leading to and from a flow meter actually becomes in integral part of the meter and thus influences its natural mechanical fre quency re ponne Obviously it always low crs it A high fidelity flow meter when inserted into long rigid tubing used for the cannulation of a vein is contcrted into a low frequency instrument unsuitable for faithful rccording of the flow pattern Summar.ing Quantitatnely accurate me asurement of rapid flow changes in cins is diffi cult due to the folloning facts (1) The high flow accelerations requno in struments with a high natural frequency re ponsc (2) The small preure licad available in icins cxclude or limits theu e of flow meters with an inherently largc resistance (3) The collap ibility of veins necessitates the establishment of 1 reproducible or known cross sectional arca of the vessel (4) The use of tubing conducting blood to and from a flow meter is Imuted beciuse it ini distort the flow pattern by reducing the a cmbly s frequency respon c DIFFERENTIAL PRESL RE FLON VETERS If a pre sure difference is created by introducing a fixed device between two points in 7 streaming fluid thus difference will vary in proportion to the vclocity of the fluid The pre ure difference can be created in various u 138 as illu trated in Fig 10 ·1 VETHODS TOR VEVOUS FLOW MEASUREMEVT 35 U 100 mm H2O D IDO 60 mm H20 60 RESISTANCE METER VENTURI METER ENERGY LOSS BY FRICTION ENERGY LOSS BY FRICTION U 100 D ប 100 D 80 60 LAT ERAL 60 ORIFICE METER PITOT METER PRESS 此 C ENERGY LOSS BY FRICTION ENERGY LOSS BY FRICTION FIGURE 10 Schematic diagrams allustrating the creation of pressure differences in streaming Ruid for measuring velocity of flow by differential pressure manometry U = upstream manometer D = down tream manometer Difference of hy irostatic pressure in side tube manometer is symbolized by the fiud les el in mm of water Energy low by friction 19 plotted as a broken line below each type of differential meter Descnption to text (a) Resistance flowmeter Narrowing the lumen causes friction thus poten tial energy is lo t The lateral pressure on the wall above the area of constriction 13 higher than below the narrowed part (Fig 10A) Application of this prin ciple alone is not practicable in the venous sy tem because of the high resistance necessary to produce a sufficient pressure drop Each of the three other devices (B C D) shown in Fig 10 also offers some resistance and the pressure differ ence created by them is due to the fact that they act partly as resistance flow meters (b) I enturimeter Essentially a venturimeter is a wide tube which has a short constricted segment (Fig 10B) In the ytde part velocity is low thus the potential energy which creates the lateral pressure on the wall is great and the kinetic energy (energy of flon ) is small In the narrowed segment blood flows faster and potential energy is converted into kinetic energy The downstream manometer tube at the con tricted area registers a lower lateral pressure than the upstream tube Beyond the constricted area kinetic energy is reconverted into potential energy The energy loss on ing to friction is small This very re hable method had been widely used in technical applications but was not em ployed by physiologists until de Burgh Daly (1926) \\agoner and Livingston (1928) and Lauber (1928) used it for measurement of blood flow ·36 EVOL RETUR In our laboratory se successfully used 1 large bort venturimeter of our own design (Fig 39) for measuring pulsatile changes in inflow into the central veins (Brecher et al, 1932) This instrument combines adequate sensitivity with low iesistance and absence of turbulence up to flow rates of 720 ml/min Its frc quency re ponse is approximately 40 cycles/sec According to Green (1948) a Ienturimeter does not register flow reversal Honcer, the instrument wc uscd recorded reversed flow (c) Onfice meter When a tube is narrox ed at a point (orifice), the streamlincs continue to converge beyond the orifice (Fig 10C) Lateral pressure is mix imally reduced dou nstream from the orifice at a distance corresponding to lialf of the tube s internal diameter Therefore the downstream manometer is con nected to the flowmeter at this point Interchangable plates of different orifice sizes (Gregg and Green 1940) or a variable screw wluch narrows the lumen (Shupley et al 1943) permit adjustment of the cnsitivity The orificc meter las been widely employed for studying the phasic flow pattern in arteries (Reissinger 1928 Gregg and Green 1940 Shipley et al, 1943 Introwitz ind Kantrowitz 1973 and others) We were unsucces ful in using Greggs or whipley s original devices or modifications thereof in veins The sensitivity was inadequate when large orifices of low re istance were used wlule small onficcs introduced too much resistance Furthermore the range of flow rates free from turbulence * 18 very narrow (d) Pitotmeter When a Pitot tube with its open end directed upstre un la inserted into moving fluid the energy of movement is added to the existing potential energy (pre sure on the wall) and a lugher net pressuru is recorded in the Pitot tube When the opening of a Pitot tube frecs downstream the hinctic energy of noi cment is deducted from the potential enerbs (pre surc) The Pitot cffect results in a difference between the liy drostatic fluid les cls of the upstream and downstrcam Patot tubes This is symbolized in Fig 10D Here the potential energy of the fluid reservoir (to the left of the drawing but not shown) corresponds to a column of 100 mm of water In thic tube of flowing Inquid potential energy (w all pressure) amounts to only 80 mm lateral pressure 19s indicated by the strught manometer to the left) When the kinetic energy of flow us reconverted into potential cnergy it results in a column of 100 mm of water (80 + 20) in the upstream Pitot tube (1hich faces the current) and of 60 min of water (80 – 20) in the downstream Pitot tube In this example the energy low by friction is neglected Compared with other differential flow incter Pitotmcters produce le-res tance-and thus less cnergy loss by fric tion—for any given pressure difference created for this reason they appear best ad aptable to venous flos measurements The det ulod study of Patot meters by Alois Vuller (19a) cncourage their use in future cypurinentation The fir t Pitotmctor for blood flou vas constructed by Cybulski in 188) molific d by hii nchi in 1923 and finally applıcd by Fich in 1934 for venous flow regitration The e uthors projected the menrei of the upstream ind down tream Pitot tubus eparateks on a photohy mograph Their flos cannula s is bulky and the inertia of the unit made it unreliable for pla ic recording other than lou change of venous fou i ociated with ri piration In Fig 11 tuo Prtotmeters are hown which has been successfully employed

·mm
ETHIOD FOR EVOLS FLOW VEA LREVENT
37
in studying plia ac changes of flon in the central veins They are used in con
Junction with a differential inanometer (sue also Fig 12) in order to product
A more atisfactory frequency response than Cybul bi and Fick obtained The
deuce shown in Fig 114 was des cloped by Eckstein, et al (1947) to mea ure
inferior cna caval flor in an open chest normal dog and in hemorrhagic shoch
Idequate sensitivity could only be obtained by providing the niall hafile plate
D
Y
Planung
TO UPSTREAM SIDE
OF MANOMETER
TO DOWNSTREAM SIDE
OF MANOMETER
PERIPHERAL
END
CARDIAC
END
scale i mm
0
5
10
15 20
FIGLRE 11 Schemata diagrams of two types of Pztotmeters used for measuring for in the
reae csiae Top flon meter emplos ing a bafie (1) for macrousing the presure dutierence
(redrawn from Ebstein liggers and Craban 1911) Bottom torte lo hapet flowmeter
with good streamliging et aracter tics (1{exter 193)

·38 1 EVOLS RETURN DIFFERENTIAL PRESSURE MANOMETER HEAD OF CATHETER FLOWMETER RIGHT ATRIUM A ATRIAL PRESSURE SUP CAVAL FLOW- MANOMETER FIGURE 12 Schematic diagram of Pitot type catheter flowmeter and its manometer connec tions The flowmeter head is shown restiog in the superior vena cava the walls of which are rypanded from the inside by a bashet Description in text on the upstreum Patot tube This renders the instrument insensitive to flow in the reverse direction (backflow) The natural frequency response is ap proximately 45 cycles/sec Since Eckstein s instrument is bulky and does not permit chest closure our laboratory developed the small Pitotmeter shown in Fig 11B (Viter, 1993 Brecher and Mixter 1953) It has a streamlined body in the center of the flon cannula to reduce turbulence The upstream pressure pickup is funnel shaped the downstream pressure pickup forms the narrow tail of a torpedo like body This device permits recording of forward and reverse flow without turbulence or cr a range of flow rates from - 1200 to +1800 inl /min when used in dimen ions fitted for the caval veins The resistance is small and no bulging of the cava on the upstream side of the flownicter was observed Unfortunately the natural frequency response of this instrument with the tubing leading to the differential pressure manometer ranges only from 8 to 35 cycles/sec This suffices for recording re pirogenic flow changes but is too slow for faithful re cording of the fast variations of flow that occur during the cardiac cycle In Fig 121 Pitotmeter is shorn which can be introduced as a rigid catheter into the large intrathoracic cavae without severing the ve sel or opening the che t (Brecher 1933) The catheter flow meter consists of three tubes labeled 1 U and D The end of tube 1 lies in the right atrium and transmits the atrial pul es to an optical manometer depicted in the lower left section of Fig 12 The end of tube U faces up tream whereas tube D is directed downstream The pros ure difference activates a differential manoincter (upper left Fig 12) Tlie catter head is held in midstream by five stainlc s stcel prings which can be (ypanded by turning 1 screw it the catheter handle after the catheter & inser ·AFTHODS FOR VENOUS FLOW MEASURENEVT 33 tion Use of the catheter fton meter reduces the necessary operative procedure to jugular vencscction only Volume fion can be quantitated owing to the fixatron of the seu els crows sectional area by the basket expan ion Becauve of the long catheter tubing the natural frequency reponse ranges only from 15 to 30 cycles/sec This in trument has been used successfully for studying respirogenic changes of croUS turn A limiting factor of all differential pressure flon mercrs described above as the optically recording diffcrential pressure manometer This device was first de signed by Otto Frank in 1899 modificd by Fleisch in 1920 and later improved by Gregg and Green (1910) Even in its latest form it is cumber one to work with and at reduces the frequency response of the asscmbled apparatus because of the liquid column in the tubing leading from the flow meter to the manometer The chematic dingrun in the upper left part of Fig 12 illustrates the prin cipit of the dificrential pressure manometer The high upstream pressure U symbolized by a heavy arrow is transmitted to the inner saline filled chamber of the manometer Thc lower dopo trcim pres urc D symbolized by a small Arrow is conducted to the outer aline filled chamber of the marometer These pressures act from opposite sides on a thin rubber membrane which is hence de formed by the prc sure difference The membrane cxcursions are recorded from 1sniall mirror on the membranc Light reaches ard leaves the mirror through 3 glass window m thic outcr chamber Summar ing Diffcrential prc aure fowmeters using the Pitot principle appcar more suitable for cnous fox mcasurement than those based on the resistanre Venturi or orifice principles RECEVI DEVELOP SEYTS Attempts have been made mucently to improve the fidelity of differential pres surt fon meters by using clectrically operating manometers Tlus helps by re ducing the length of the Aud columns Muller Laszt and Pircher (1948) de cribe a differential anometer with clectrical transmission suitable for flow recoriling Biter ind Pe urse (1901) de clored a rather complicated condenser differential manometer for measuring fox in the pulmonary artery with a Patot mcter It could be adapted for ycnous fou recording Nilsson and Kramer (1904) construrteu a Venturimeter which they inserted into the inferior vena cava (Fig 13) The pressurt difference is created by de srca ing the internal lumen of the fion meter tube (a) by 1 This introduces sonjere i tance to flow and creates ipinimal turbulence The pressure difference (electrical ignal) 1 houver small and requires grcat amplification Pressuns uc corducted through furl short ur tre.mnd downstream manoineter tubes to a differential minometer utilizing the strain gauge principle The frequency lepon ( of the entire gescmbly is limited to 30 cycles/sec at the amplifiers output circuit by a sers schstic and hence slonly responding gal anometer Thu howcier could be improved upon in the future Tuc differential conductance manometer of Pappenheimer (1904) could be ·10 I ENOUS RETURY b с FICURF 13 Venturtmeter and strain gauge differential pres ure manometer for mca mement of volumc pul es in central seins a = lenturimctcr b = rigid upstream and down tim manometer tubes connecting Icnturimeter to differential minometer c = strun giugo differential manometer d = stopcochs for flushing and checking of zero flow (1fter Mon und kramer 1931) applied to recording of pha ic flow in icins when used in conjunction with uit able pres ure pichup devices Its natural frcquency is higli From a lemodynamic vicu point the best constructed Pitotineter is the electrical differential manoncter of Betticher Vaillard and Vuller (1954) which has an excellent frequency re ponse and great sensitivity Summarı ing Replacement of the optical differential manometer by electrie al pickups can improve the fidelity of differential flow meters CRITIQUE OF DIFFEREYTIAL PRESSURE FLOW VETI AS Differentil pressure flou incters have 1 nonlinear calibration The flow ignal reflects the squire of the flow clocity This makes the computation of volume by integration of the tow trueinga laborious and limits their ure for timing flott curics with a ziro phie (For various 0661 tione cc creen 1918, Vitor 1933 huntronitz und hintrowitz 19.3) ·NETIIODY FOR VENOUS FLOW WŁASUREMENT Differential fon meters confront their designers with the same dilemma iacing Engineers in high fidelity recording of small rapid pressure fuctuations If the phy ical force (signal) 19 «mall the gain of the recording instrument must be greatly inereascd by optical or electrical amplification The amplification however islamited by the signal to none ratio Thus af enwronmental brı cions (for optical recordings) of clectronic sore (for clcctrical aplification) become so large that they begin to distort the agnal the practical limit is reached The problem cannot be attached by making the mechanical devices (fos cadnu lac membranes gahanometers) Extremely sensitive because their fregucney response decreases wien sensitivity 18 increased The range of compromise be tuen adequate frequency responst and sensitavaty 1s 1 cry narrow when differ entral Nou recorders are used in the senous system A scrious challenge to the validity of fox measurcraent by differential pres surc flow meters has been solced by Spencer and Denison (1906) and by Richards and Illums (1953) Using an electromagnetic flow meter they could got confirm the custence of a phasic fox reyessal at the end of systole in the carotid and femoral arteries as had been reported by Shipley et al (1943) who worked with an orifice miter llien Richards and lillsams produced a strong resistance to flos by applying a cuff dıtal to the electromagnetic flowmeter they created a flow pattern slowing the recrc flow which Shipley et al lad demonstrated They concluded that the bach fon recorded with an orifice meter may be an artifact produced by the resistance of the flow meter Their deduction honeser may not bcald Tihen an inflatul cuff sapphed around an artery distal to the electromagnetic low meter the csscl segment be tween flow meter and cuff distends during systole like a compreseson chamber During diastole the clastic force of the distended arterial wall causes a local reflux of blood through the electromagnetic fonmeter Actually the restance produced by a differential flow meter is not dsstal to but right at the points of the pressure pickups This would cause a di-tension of the arterial vaší proximal to the floxameter and hence could not produce back for tlırough the flow meter durin, dsastole Since t)s is an essentir question concerning the accuracy of pha-se flox mcasurements in arteries as well as 11 cins notcr cxplanation should be ought The apparent bach flow could be an artifact created by the acceleration fac tor in the differential quotunt of Otto Frank (1929a 1930) At high for ac celeration this factor can increase the signal deflection beyond the actually existing loss selocitas This Signal deficction for differential fon meters depends not only on the clocity ( kinetic energy factor ) but also on the rate at which the vclocity chane ( aceeleration factor ) If for example the flow velocity cerca ed uddenly at the fir • prebure pickup the fluid column between the tuo mcusuring points sould still communsente and owing to its inertia thug blood would ccrt (xcesive pro- ure on the wecond measuring point This should not occur of both pickups ire in the 4311e cross sectional plane of the sesael By 451198mg Pitot pres ure pickups in the same plane Alors Viuller and luis 1ociato (1918 19 ta) demonstrated that the eccleration factor and thus any brek fox artifact would indeed bocorre insignificant The Pitatmeters u cd in the experienta rcported here "uffered from an orcr ·12 TE VOLS RETUR.S shoot' of the signal deflection caused by the inertia of the manometer flud col umn and by the acceleration factor For this reason records taken with these instruments permited the study of slow respirogenic changes of flow but not that of fa t cardiogenic changes Since the or crshoot was empirically deter mined to be of approximately equal magnitude in both directions (for forward and backward flon ) it could be cancelled out in the analysis of the records for slow changes (Vaxter 1903 Brecher and Inter 1993, Brecher 1903) Summarising Adequate construction of differential flow meters can minimize or aboli h the acceleration factor which otherwise may distort phasic flos curses and mu late a bach flow PENDULIV ILON VETERS The principle of the pendulum flow meters con ists of the introduction of 1 small pendulum paddlc recd wc or bristle into the bloodstream The flowin.. blood deviates the pendulum from its resting position The deviation is propor tional to the velocity of the blood stream This hy drody nanjic principle was introduced by the Italian engineer Ca telli (1577-1644) a student of Galilei (Vuller 1951b) Vieroidt applied it in 1838 to the measurement of blood velocity (lny dromctric pendulum) Chauv cau (1860) and lus student Lortet (1867) des cloped the hemodronograph with which they recorded pha ic flow and prensure in arteries simultaneou ly The principle was agun advanced in Otto Frank (1928 and 19296) but not further employed untıl de Burgh Daly developed in 1930 1 flow meter which measured electrical capacity changes induced bs shifts in pendulum po ition Again the informa tion was forgotten and remained unknown to Bergnian (1938) Holzloliner (1938) and Holzloliner and Schoner todt (1940) lien they descloped their bri tle tachograph They measured the electrical resistance between the plata num tip of a moscable glass bri tle and fiscd plitinum electrode in the flow cannula this resistance varying with changes in the amount of blood (di tinci between the contacts By using the curviline ir linb of the bridge balance curic thic produced a lmear calibration curic Unrcliable drift ind uncontrollable rt istance changes due to minute fibrin depo its or other impurities at the pliti num tip of the bristle are the main obụection to this mcthod (For critici moc Pilper and letterer 1933) (3) Electromagnetic pendulum In electromagnetic pendulum flow meter the pendulum is inide of ferromagnetic material which mores in an induction field The inductance changes are then amplified llc constructed soon the flow meter of this type by winding the induction coils of 100 turns cach around a plı tic cannula ito wluch 7 pendulum cight a lon, containing approumatuks 100 mg of iron protruded (Crum 1932) The signal to noi critio was lugbinddrift due to temperature changes atnounted to as much as 10 per cent of the ignal strength Scher et al (1903) constructed a similar dene u ing a paddle shaped ferromagnetic pendulum with only for coil winding resulting in lou «n tists but good tumperature stability Pieper ind Wetterer (1993) soked the tability problem rucce full by ·VETRODS FOR 1 EVOLS FLOW WEASLEEMENT 43 BLOOD FLOW MANOMETER 913 A B FIGURE 14 Schematit diagram of electromagnetic pendulum flowmeter for mantou nitasurement of flow and pressuse A = Cross sectos slowing a mature manometer absorted at the side of the T segment of the fan-caudus B = Cross-section at 50 is I shossing arrange cbt of electromsyset and honzontal segment of T-cannula uch us berted into bloor eevel Decule I = piluction metal 1 ferromagnetic core C=coil P-pla tar con er and 1 wateh spring Proportion not to seale Mamal dimensiot "am Redrann from Pseper and Wetterer 1953) placing the iron mass in er part of a long pendulunı » protrudes from a T cannula into the blood trcam (Fig 14: The induction coils are wound around the vertical part of the T caunula and are not much affected by tempera turc changes of the blood much streams through the horizontal part The natural frequency of this fion meter 38 200 cz cl£s/sec Though employed by Preper and 1Vetterer in arteries this instrument mould be very surtable lor enous fion re cording sitice it offers practicalls de resistance to flow is senstue and of small dimensions Unfortunately the intricate flow densing element must be home made (b) Bristle flou meter Vany studies reporter in this book were undertaken with the aid of the briatic flow meter destloped in our laboratory (Brecher and Praglin 1933 Brecher 1931) The fios ensing clemcıt 35 4 subminiature rac uum tube (Radio Corporation of America lo 5734 mochanoelectronic truns ducur) The great constructional advantage of this bristle for meter is the cora inercial availability of the flos senting element which merely needs to be incorporated into a suitable cannula Scher et al (1953) simultaneously con structed the same type of lon meter schematic diagram of the bristle flos meter is shosa un Fig 15 The 9736 tube is held in 1 «cres base it and I Part 1 connects the teren base with the ·14 VEVOUS RETURA FLOW z K 5734 wwwwwwwww pat W M SIGURE 13 > hcmatic diagram of ba tle flow meter cannula utilizing a 5*31 subminiature vacuum tube is flou un ing element Total length of cannuli w0mm Dc cription in text licad of the cannula Z which is inscried into and ligated to the vessel 'Heads of rious dimcn ions can be used with tlic simc flow cannuli for different sized Posel sud tube a series for removal of air bubbles, fluslung und pressure re cordin, The blood stream deviates a sinall bristl (B) which is attached to the platc pin of tlic jacuum tube Thc bri tle acts 18 1 luser ind its deviation is pro portional to the flow vclocity The plate pin eXtends through a flexible met al dia plıragm into the inner part of the vacuum tub. The metal duphragm thus acts as a fulcrum the inner part of the plate pins thic inode 1 hen the bri tic is desiate the electron current from cathode to inol i trics in proportion to the distance betrcan tliem which is determined by the dece of desnation The electrical anal is implified and recorded with a suitable high frequency mirror gik inomuter on 1 photos 100 rapa or sith anotlıçr incloating device ·VETHODS FOR VENOUS FLOW MEASUREMENT The natural frequency re ponse of the 5734 tube is 12 000 cycles/sec The response is decreased by attaching the bristle the decrease depending upon the length and the mus of the attached piece Using a filament about 38 mm in length a natural frequency re ponse of 129 to 200 cycles/sec can be attained In combination with a specially designed amplifier and power supply the bristle flow meter has 1 cry little clectronic drift and a bigh signal to noise ritio lith out decreasing thic high fidelity of the moving mechanical parts of the instrument the pulsating flos signal can be electrically integrated in the amplifier circuit (Praglin and Brecher 1955) The bristle fos meter has the following advantages which make it e pecially suitable for recording rapid fluctuations of flow in veins (1) negligible resistance to blood flow (2) high fidelity (3) great and Variable sensitivity (4) compactness (5) ahsence of turbulence over a wide range of flow ratus (6) equal response to forn ard and backward flow and (7) negligible ba line drift A K 5734 B M FICE RE 16 Cross section of pristle fowmeter mo bficu for ure in the pulmonary arten trunk for determination of the right heart trohe solume Total length of aagula 5 mm De erup tion in text ·16 LEVOUS RETURV A special modification of the bristle flow meter las been developed for direct according of right cardiac output (Brecher and Hubas, 1901) This enables simultaneous study of the hemodynamics of cardiac inflow and outflow Figure 16 shows a diagram of the flowmeter cannula and Figure 17 an artist's concept of its position in the pulmonary artery The device consists of parts A, B, and C The tip of part A in inserted into the vessel wall by slipping the lip D through a "buttonhole" opening in the arterial wall Lip D is sccured to the intima by the pressure of plate E on the outside of the wall Plate & is lield in place by scren F A cylinder G can be pushed forward or ictracted by means of a cable release II When the cylinder G is in thic ictracted position is shown in Figure 16, the H K PULMONARY ARTERY TRUNK AORTA RIGHT VENTRICLE LEFT ATRIUM 17(LE 17 In tu diagram of the bristle flow meter which is depicted in ligure 16 Italiu trate the flowmeters i osition in the pulmonary artery II = cable relca-c for advancing anle tracting zeroing cylinder h = ale tube for recording reasures and removing airbul i les I = bristle and \ = metal bund sabieh fires the circumference of the ulmonary artery this us pussing around the col The zeroing cylinler is not vible because it a retructa 1 ·METHOD FOR EVOU FLOR MEASUREMENT 17 bristle I can bc derated by the blood stream I hen the cylinder is pushed for Ward beyond the bristle tip it protects the bristle from deviation by the current This cylinder for producing zero flow has proven to be very valuable for main taining physiological circulatory conditions It permits frequent inscribing of zero flow in any segment of a record to check on electronic drift without the neces its of interrupting blood flos bi clamping the vessel This is particularly important in the pulmonary artery trunk where temporary occlusion of the Vessel may overdistend and damage the right ventricle Pulmonary artery pressures are obtained through tube A Part B is a long threaded shaft into which part C can be advanced by turning Part C series as a socket for the RCA 5734 vacuum tube 11 indicates the leads to the recording instrument The bristle is protected from damage during the in ertion by turning part C until the tip of the bristle is retracted behind lp D After in crtion through the pulmonary wall the bristle is advanced into the lumen of the pul monary artery by turning part C A metal band is placed around the vessel in order to fix the artery s diameter as illustrated in Figure 17 This is indispen cable for quantitative flow measurement. The flow meter must be calibrated in situ after the experiment The advantages of this modified bristle flow meter are the following (1) It permits faithful recording of pulmonary artery flon and its fluctuations from one heartbeat to the next (2) It can be inserted with a minimum of trauma into the pulinonary artery trunk without blood loss and without interrupting flow (3) Since the clectrical mean averages all actual forward and backward flow at the site of the flow meter it records what is conventionally defined as cardiac output A typical calibration curve of the bristle flow meter is depicted in Figure 18 The calibration curvc follows approximately a square function (For details concerning the relation of bristle deflection and fluid velocity sec Vuller 1984b) The calibration is done either in situ or with the aid of tubes by passing steady or pul atile currents of blood from a reservoir through the flow meter The cali bration curve must be empirically determined for each experiment As designed in the amplifier (Pregion and Brecher 1955) the calibration for pulsatıle and average flow is identical This permits stitching from the recording of pulsatile to mean flow during the caperiment (c) Strain gauge pendulum flou meter A strain gauge wire 8 mm long is firinly fastened to trapezoid shaped pendulum 4 mm long The deviation of the pen dulum stretclics the strain gauge wire and the ensuing resistance change is used to produce an electrical signal The main advantage of the instrument 18 its small size It can be adı anced through a 13 gauge needle into the vessel to measure blood vclocitics Though the instrument is still in a developmental stage at may have a promising future (C R Hong personal communication) Summarı ing Among the various pendulum flow meters which have been des cloped, the 5734 bristlc flow meter utilizing commercially available parts, is the easiest to con ·18 TIVOL RLTUK CC/MIN 27001 2100 1800 1500 1200 900 600 300 50 100 150 200 250 MM DEFLECTION FICHE 18 Chrition curse of bristle flownieter For flow in the reverse direction the cun e 15 symmetri il to the cure for forward flow struct It peruts futhful 1ccording of rapid flow changes in vcns of experi mental animals CRITIQUE OF PINDELL V FLON VETERS For evaal rea ons pendulum flow meters have enjoyed little popularity in the past but hac recently been judgid quite useful 1 Their in itauts depends principally upon the form of thic pendulum Tho larga the ob truction to fon the greater the cn ituty but the poorer the fidelity becauc of the pendulum mans If the ob truction is large as by a biord puddle the deflection of the pendulum is approximately proportional to the squire of the clocity The resulting calibration curyc is thus nonlincar If tlic obstruction a Vy imall 13 by a tlun filiment the deflection of thic penduluin is almo t proportional to the clocity and the calibration curse appioaches linearity i ce also Vuller 19,1b) a uitable pendulum usually incorporatis a compromise between sufficient en duty ind adequate frequency re pon e In the licinodromograph of Chiuvenu and I ortet lugli fidclits ind lon re stance had to bc sacrifica in fhor of sufficient sensitivity This dilemma could not be ovcrcome until very sensitic electrical transducers were de cloped The bigh sensitivity of the 5734 Subminiature vacuum tube and Picpers and letterer s electromagnetic transducer has given a special impetus to the desclopment of modern pendulum devices 2 great ads antage of the pendulum flos meters is their mall size and com ·VETHODS FOR \}\OLS FLOW VEAST REVE\1 19 pactness The segment of the cannulatcd vessel wuch is fixed by the ring like structure of the cannula head is only a few millimeters in length This assures a minimal interfcrcnce with the normal flow dynamics The instrument can be ca il in crted into short segments of ve is in tight corners the chest ab domen or other ti ucs can be clo ed and resume their normal anatomical po sition 3 The acceleration factor of Otto Frank lich plays an important role in differential pressure flow meters (see page 411 is negligible in pendulum flow inctcrs 4 A disadvantage of the pendulum flow meters is the weight of the pendulum itself In a sensitive instrument gravitational effects created by an alteration of the position of the flow mcter produce a change of electrical signal The instru mcnt inust therefore be firmly clamped during an experiment 5 Further disadvantages of pendulum flow meters are the necessity of using anticoagulants and of opening the ves el for the insertion of the bri tle With adequate heparinization and coating of the in trument with silicone we have never observed any fibrın depo it on the bri tle or flon cannula Summar ing Pendulum flow meters harc adequate sensitivity and fidelity only by virtue of very sensitive tranducers Compact pendulum device do not distort flow dynamics The necessity of cannulization limuts their use OTIIER PHASIC FLOW VETERS Brief mention should be made of sci eral other flow meters which have not yet been used for accordin, of phasic changes of venous flon but which offer future po sybilities (a) Electromagnetic flou meter Electromagnetic flow meters have bxcen used succoy fully for pul atile flow recording in arteries (holin 1936 Katz and Kolin 1938 Wetterer 1937 Wetterer and Deppe 1939 Deppe and fictterer 1939 1940 Wetterrr 1940 1954 Jochim 1948 Richards and Williams 1953) The main disadvantage of the electromagnetic flow meters is their lon signal to noise ratio One must distinguish three types of electromagnetic flos mcters (1) The direct current meter This was used in various forns by holin (1936) Wetterer (1937) Jochim (1918) and Richards and Williams (1953) It suffers from an interference of the flow signal hy random polarization voltage (2) The sine uare current meter kolm (1941 1945 1932) removed the polarization of the electromagnetic field by applying a sinusoidal alternating current to the magnet However the alternating currunt induccs in the electrodes a voltage which inter feres with the flow voltage (Richardson Denison and Green 1952) (3) The square uare current meter Denison Spencer and Green (1905) oi crcame the difficulties of the szne ware current by applying & square ware alternating cur runt The magnetically induced voltage from this current forins induced pics which are removed by a chopper in the amplifier Spurious voltages and inter ference by clectrical artifacts (ECG) have been greatly reduced by increasing the magnetic flux (saturating the magnet) and by increasing the square ware ·0 TE VOLHETLI alternating frequency In its latest version the flow meter permits futhful rc cording of plac flow, as it has in upper linut of frequency reponse of aver 100 cycles/«ce (Spencer ind Denison, 1992) The eletrom ignetic flow incter mycts with cont difficulties in the schous sy tom pırtıcul irly in the central vins In arturica, the finn clectrode applica tion is i sund by i buntk compression of the it In the collap ble veins such procedure sould not be fua ible It imy hokuser bu proible to fix thic cro sectional itu md po ition of the son in the magnetic field by urrounding the res cl with a ring lihe suction lucie uluch presents collap c of the walls Strong ECG currents may al o interfere with the flow ignal in central veins Tuscrtielony the great adi intibes of the electromagnetic flowmeter pecially in its late form (Spencer ind Deni on 190) may make it the in trupent of choice for the futurt Its main dut bls art (1) quantitinc measurement of phasic flow in intact ic cis without the use of intico igulants (2) lancar calı bration (3) cqual reponse to forward and bachard flow, () mall izc and cumpactnes of the flow sensing unit bi Drathormy thermostromuhr Ilus method and come una arranted claims w duchlie di credited the thermostromulir for u c at the unopened ve I were di cu cd in detail by Gregs (19481 Iven the modification and improvement of the thermo tromuhr by Oberdorf ind Ilalche (1924) have not removed the inherent calibration difficulties les per pective basc been more recently opened by reinvestigation and modification of the thicimostromulir principle Following study of 1 choff (193)) on the heat transfer to streaming blood Vau 11900) Ichoff ind over 1196) ind lever and Ischoff (1996) m vc tigited the applicability of the deathermy thermo tromuhr to unopened ve els l nga diatherius frequency of 200 to 300 hilocyclonec they found that 80 per cent of the cnergy goca to heat the wall and not the blood column The wall is warmed symmetricalls that 1 more down trcim than up trem The heating of the up trcam portion of the wall is little effected by the blood flon Houcier thic downstream tenperature depends orently upon the volume flos of blood munls beciu blood cools the donnstram portion of the reci wall The temperature changes ue rapid but till too slou for futhful recording of very fast changes in blooflow Though the ignil to noise ratio of the dar theriny stromulir is better than tint of the square #lic clectromagnetic fox meter it may be less applicable to central veins becau e of the slow response Probabls its best suited function is the measurement of flox in unopened peripheral ic els (c) Catheter thermo tromuhr Inother accent modification of the thermo stromuhr appears promising for 1 enous fon recording in larger unopened vessels Lanzon (1955) constructed a thermo tromuhr which is incorporated into the tip of a catheter It can be in crted from the citcrnal jugul ir iein into the coro nary sinus of 4 dog without opening the chest Six short heating clements in the wall of the catheter tip are cooled by the coronary sinus blood An inflatable balloon near the catheter tıp insures that all coronary sinus blood passes by the thermodes The blood then druns from the catheter lumen into the right atrium through holes in the catheter wall Thus trument also in its present form suffers from a linutation of frequency response ·VILTISODY OR TEVOL FLOU VE LREMENT ul (d) Thermistor for meter A different type of a thermostromuhr is based on the principle of thermistors which are cooled by the streurning of blood The thermistor fon meter of Fell and Groll (1933) and Felix (1935 1936) has a number of advantages The flor sensing element the therimstor is commercially Alnable (Phillips Co) The thesmi tor 18 4 very small resistor which alters Its electrical resistancca with teruperature eh ungs The mass of the thertor Is o minute that when it is innerted into the blood stream the element responds fully to a temperature change within 1/20 sce The thermistor forms one of the irtos of 3 Wheatstone bridge Oning to the extreme sensitivity of the douice for clou flows no amplication of the signal 18 necded Zoro drift of the baseline is ab ent It is ideal for the study of minimal fows The disadt antages of the desce are as folloss (1) It cannot distinguish betueen fort ard and backward fon (2) The calibration la logarithme shoning grert sentity for los flow and little cusztrity for high flors Thus the trac ing for zero flos cannot be included on the record and the calibration as cumber sowe (3) The ver ci mu t be cannulated for a considerable distance for calt bration purposes levertheless ouing to its great simplicity and sensitnity the thermistor flow meter may become a suitable instrument for the measurement of small flow volumes in peripheral se cels of experimental animals when the pos a bilty of back ion is excluded (es Electrosonic for meter The electrosonic flow meter can be used on un opened sessels (halmus 1951) It is based on the principle of the phase shift of ultrasonic sound at different fion sclocitres It is moderately compact has ade quate sensitivity and a high frequency respon e The electronic cignal detector is rather coupiscated Theoretically the instrument should have good prospects for cnous flos recording Sunimart ing The electromagnctic and electro puc foxmeters may perind recording of rapid phase flow changes in unopened seins The duathermy and catheter ther mostromuhr appear suitable for measuring moderately fast changes of ion in unopened ress The thermistor flow meter is very sensitae and stable for record ing of small volume flos in cannulated veins I DIRECT VETHODS Except for isolated problems indirect methods do not at present furnish suf ficiently accurate information for quantitatise study of sersous return How ever mestigators sall always true for perfection of indirect methods because many instances these are the only ones 5 hich can be applied succes fully to human beings and animals under physiological conditions Smce it is beyond the scope of this tono,raph to resses the literature on the rapidly progres and highly technical subject only a few recent adı ances should be painted out which open new perspectnes (For the older Iterature see Franhlia 1937 ) In the future the answer to many questions 1713l be prouded by high pred direct and x ray cinematography of the movement of blood m veins (For tech nique and results consult Bohme 1936 Laszt 1949 Gohrbandt et al 1993 Lind et al 1955) The quantitation of the clocits neasurements in terms of ·TEVOL II TLILS volume tlou utieis particuludy datle ult problem (cDonald, 1952 Hcps and VIcDonald 194 VcDonald, 1934 VicDonald 19 », llormersley, 193» Hall, VcDonald ind llormer luy 197) and pus on il communic ition of VeDonald) In udition to their rom ith able contributions McDonald ind his co workers he il o pointed out the technical dilliculties ind limitations of the pire ont cinematograpluc methods of ingiography Introduction of forujn material such 19 ur bubbles sodopine drop uic for fou quantitation meets with stral theoretical objection Quantitation of pul ntile volume flow is best accompli led by an inils is of the moving front of the injected material (dyc or riy opaque flud) Only at the region are differences of optical den its between blood ind the contra ting material trong cnough for u ualization Ilower the border of the contrasting med i very industmet The borderline become cien more diffu cd by pul atile vclocity changes ( 119) During period of foru ir flox (116 191) thu paraboloid cone of the awal stream greatly pricedes the inarginal stream Ilhen the fluid column ruces during a period of bichward flou (1 16 193) the flou reser al is greater for the awal stream thain for the inirgin Thus looking tlırough the intact vesel from the su prrt of the iwal stream ippairs to be cnseloped and con cuntis ob A Fluth 19 To valization of the optically diffu e border in the flow profit of contrast matemal in a ve sel during (1) forward flow and (B) a brief period of bieku ard fox The Norm xhons only a section through the longitudinal mdpl we of 1 hentie ien I (Deuring based on concepts (1 olie 113 McDonal!)

·VETHOD FOR IETOL FLOW VEILREVENT 3 scured by the dense cylinder of the marginal streuen which undergoes little or no backward movement The croection in Figs 194 and B should be visualized three dimensionally to appreciate the difficults of trrein, the movement of blood through the cro scctional area of an intact as e pecully if the sensel chan,es its shape from moment to moment For fion quantitation in reins sterco cinematography or taking pictures of the ve sel froin tno planes at right angles may offer lytter chances for analy 1s Further progress in high speed ray Cinematography of unexpo id ve sels in situ inay be expected by the cisployment of special cameras (Golirband et al 1933) and of ray interstiers such as those made by Pallips and I)esting house (Lind et al 1925 Irdran und Wyatt 1901) Suinnarz ing Quantitation of phasic ion chan,es in veins by the use of indirect methods is technically difficult becau e at present it is not po ble to obtun the neces sary preci son for visualization of changes in volume flor ·VI Venous Hemodynamics Tlie special features of venous llos dynamics are mostly due to the collapsi bility of the veins For bisic understanding it is thicreſorc, best to (12mine flow through structure that a similar in shape to partially collup cd ein VopifiCATION OF POISEUILLE LAW Volumt fou through a tube or vein of an elliptic eros cctional area can be calculated by the following modification of Poiseuilles formula (A cher and Spurgeon, 1919 Vilnc Thomson 1920) + a' (p! - P3) (a + 671 In this cquition ull factors are the same is defined in Porcuilles formula (pige 11) except for rt which is replied by za at +62 Thus capression refers to the tro different diameters of the elliptic cro cctional irea a = the minor semi 2113 and b = the major scmi is of an elupe For an under tinding of the effect of the two scmi acs on flou the two extreme e zucs of an ellip C should be con dered first In a cucle (an ellip e with both sem axcs equal) i ind b would have cqual value 1 = b = r and it is readily sun thint flow through such a sein would be maximal or units compared to that through any other possible ellipse On the other hand in the flattest el Topsc (a line of thc cxtension of the myjor cu av b) the minor cm avis Hould equal zero Thus flow would be zero through a vcin with no minor tuis (completely collapsed) Hencc flou through a vessel of any cliptic cros cctional area betuen the e tuo catreme cases can be graphically represented as a function of the minor semmi axis of an ellipso is plotted in Fig 20 The tuec graphs show the elect on flow of varying the minor axis while heping constant (A) cro ectional areal (B) perincter or (C) major axis The cx amples in Fig 21 help to illu trate the graph of Fig 20 Curve A of Fig 20 is a plot for flon through elliptic tubes of con tint cro sectional arca In Fug 21 flon through a sound tube (A) 19 compared with that through an elliptic tube of the sume crossectional area (B) when the minor sem axis is decrcu id to half of unity It is noted that flow through the cliptic tube is less than half of that through the round tube although both tube base identical crossectional arcas This exaniple illustrates that 1 meie change in the form of a sessel without decrease of crosscctional arcy reduces flow It is obvious that with the cliptic flattening the major diameter must increase in order to keep the crossectional arca constant Thus kould honever not be the 4c when a sein undergocs partial collapse and the minor sem axis of its 5+ ·NEVOLS HIENON AVICS o 09 FLOW Q/T 08 1 07 06 05 CONSTANT AREA CONSTANT PERIMETER CONSTANT MAJOR DIAMETER 04 03 02 01 1 02 03 04 05 06 07 08 09 10 MINOR DIAMETER OF ELLIPSE FIGURE 20 Graphuc represeаtation of volume flor (ordinate) through elliptic tubes as a function of the mainor gems axis of the elleptic cross-sectsonal areas (abscissa) With a decrease azz the midor sem axis the area (Cure 4) penmeter (Cusse B) or mnazor sex ana (Cunc c) of the elupses are kept constant Soot sems 23 of unitt 28 the radius of a circle crossection decreases The configuration of a collapeod veta ttould correspond clo cly to an ellipse with a constant perimeter and a smaller crossectional area In curie B of Fig 20 low is plotted for ellipses of constant perimeters The cxample 38 Fig 21C shows that flon through an elliptical tube (minor cemi axis half of unity) swounts to less than one third of that through a circular tube of an xdentical perimeter (1) It should be pointed out that reias do not atnars maintain the same perimeter shen they undergo partial collapse but may occasionally approach configurations which correspond to ellipses in thich the major diameter does not change Cure Can Fig 20 15 plot for fow through ellip es with constant major semi axe. The example in Fig 21D illustrates that fou through an elliptic tube wsth a major sem w of unity and a minor edi asis of half unt; us only one fifth of that passing through a circular tube of the same radius as the major semi axis (A) From these considerations one may conclude that other factors remaining the same fos would be reduced to about fourth if during sems collap e ·56 IEVOUS RETURY MINOR SEMI AXIS mm 10 CC / SEC 47 CC /SEC A B V U MINOR SEMI AXIS mm MINOR SEMI AXIS mm 31 CC / SEC 2 CC/SEC FICURE 21 Effect of the shaj c of a tube s crosscction on flow (1) Flow through a tule of circular cross section of 1 mm radius yields 10 cc /sec (B) Tlow through tube with the same crow ectional arca as in (1) but of elliptic shape with a minor scmi axis of '2 mm yılds +" cc e (C) Flor through tube with the same perimeter as in (1) but of elliptıc hape with a minor som axis of '2 mm wields 31 cc /sec (D) I low through tube with the same tmajor sem 2013 (1 mom ) as the radius in (1) but of elliptic share with a minor semi axis of 12 mm Vields 2 cr sec Flow through a vein in a semi-collapsed state would corre pond approximately to C or if the permiter becomes maller to that through a tube intermediate butucen C and D a round sein assumes an elliptical crosscction with 1 minor scmi aus equal to one half the radius of the circular en Vlore extensive collapse of the veins than this is frequently obscrvcd It occurs rapidly or slowly intermittently or continuously as collapse is occa ioned by changes of intraviscular and extra va cular pressures (cg during the heart cycle the respiratory cycle mosc ment of the body or due to senomotor mechanisms) The amount of thc flow reduction for any degree of venous collap e can be readily estimated by con sulting the curies in Fig 20 Since flow through a partially collapsed ein (elliptic tube) is reduced lule the perfu ion pressure renuns the same resistance to flow through a partially collap ed vein must be greater than that to fon through a round sein Thus the curses in Fig 20 can also serve as a plot of the resistance to flon through elliptic tubes (icins) if one substitutes in the ordinate by 1/R (R = resi tance) As we shall see later the fundamental relations represcoted in Fig 20 serve to cxplain the flow changes through collapsing veins obscrved in no ·TEVOLS HIYOD VAVICS 07 Summar ing Volume flow through partially collapsed seins obeys approximately the laws of flow through tubes of an elliptic crosscetional area When pressure remains constant volume flow through a run in a semi collapsed state is about one quarter of that through the same sein when it is round PRESSURE GRADIET ILONG CENTRAL VEINS The pressure gradient throughout the entire vascular system from the root of the aorta to the right ventricle is very great The steepest pre sure drop occurs in the arterioles the place of the highest resı tance The pressure gra dient throughout the venous system is small since the resistance is low e pecially in the central veins Therefore pres ure differences of only a few mm of water are sufficient to drive large quantities of blood through the central veins Un questionably pressure differences of a fer mm of water uffice to drive the ame quantity of blood through the centrul veins that is propelled through the aorta since essentially the same amount of blood that is expelled must also enter the heart The extensive literature on the subject reveals the difficulty of recording ac curately the c minute pressure differences Failure to detect any gradient has even led to suggestions that there is no pressure difference in central veins Obviously this is phy iologically impossible because blood cannot flow wathout a pressure difference whatever its origin be it the zis a tergo or the ris a fronte or a combination of both Failure to demonstrate a pre sure gradient along the central venous bed may be attributed to several causes (1) As Henderson and Barringer noted (1913) the uncertainty of making reliable venous pressure measurements is due to the fact that the slightest compression or stretching of the tissues through which the vein passes is sufficient to collapse it The reading on the manomcter may thus easily be clevated many centimeters above the true pres ure or depres ed as much without the ob eri er being led to suspect the error (2) When pre sure is measured simultaneously at two points in a sein a difference of a few milli meters in the hydrostatic level of the openings of the two pres ure pickups can simulate absence or reversal of the pre sure gradient (3) Due to high peak Velocities in the central veins potential energy (measured as lateral pressure) is low and hinctic energj (energy of flow) is relatively high (see also Fig 4D) In the right atrium hinctic cnergy muy in part be reconverted into potentral energy which would result in the recording of a higher lateral pressure than in the vein Particular attention must therefore be paid to the po ition of the pres sure recording tip in veins becau e of the Bernoulli effect Semba and kishi (1953) mea urd meticulously the mean venous pre ure Gradient along thc caial veins in dogs and arrived at the follox iag cogclusion The fall in pressure of the thoracic vena cava is trifting thich shows that blood is stagnant in the central vena cava and has formed a pool The fact that the central venous pressure gradient is indeed very small can be accepted but it 15 erroneous to conclude from this obsersation that blood is stagnant Actually the greatest flow velocities in the senous system occur in the caval veins as

·co
ralan
M furt
Manometer
VENA CAVA IN
DIAAFRAGM
RIGHT ATRIUM
VENA CAVA SUPERIOR
Inspirato
comentario presenting
Sto gouge
O sec
EVENA SUBCLAVIA
أسيلسا أستبسة
VrVOUS RETURN
مرا ا ر ا ن
VENA CAVA INF
DIAPRAGM
RIGHT ATRIUM
VENA CAVA SUPERIOR
FILL RE 22 I ressure tracings from the central cins of a normal
unanesthetized person illustrating the smalas of the pressure
gradients along the thoracie inferior and suj enor senu 15 €
l'istrohes in the phase alls chidang pre- urc curses are emil
by atrial systoles Desetition in text (Original Unpublished
recorby courtce of Gauer and Sieher 196 )

·I EVOLS HEMODINAMICS 09 We hall see later The fallacy of the abovc statement mercly emphia izes that one cannot draw conclu ions about blood flow from pre sure mna urenients alone In the unanesthetized human Gaucr ind Sieher (1936) accurately recorded plia ic pressures with a very sensitive Ingh fidelity miniature manometer in order to c tablish the possure gradient along the central seins (Fig 22) Thcy pulled a double lumen catheter at a con tant rate of 5 mm / ec from the ab dominal vena cava through the right atrium up to the subclavian vein Tic flud column from the tip of the catheter as connected to i conventional strain grugi manometer, whereas the miniature momcter was situated 23 mm belund the tip llence the two senolis pressure trucings ('ind their labeling) are displaced by 46 seconds on the time scale (middle and lower curve) The curses reveal thie cu tence of an casily measurable pressure gradient from tic abdominal mfcrior vena cava through the ln er region (labeled diaphragm ) to the atrium On the other hind thicy sliow that a pressure difference of only a few mm of water c\ists botuen the thoracic portions of the caval cins and the right triumn These findings demonstrate that in manus in do, the pressure gradient along the thoracic caval veins is so small that it is very difficult to cstablı h manometrically Summarizing Owing to the low riistance a small pressure gradient sufices to propel large quantities of blood through the central veins Thus the prc sure gradient along the central venous bed is so small that it is difficult to record It can be mis leading to draw conclusions from differences of pressures when investigating volumc flow in the cins close to the heart PRESSURE FLOW RELATIONS I COLLAPSIBLE VESSELS Wc hall now consider the changes of flow içsulting from variations in pres sure gradients along veins in order to cstablish the dynamics pressure fo resistance relations during collapse of the veins in the living organism A de tailed analysis of these relations is called for since flon through collapsible tubes IS 1 subjcct which has been soincu hat neglected by physicists First a waid about the precise socaning of the term collapse which is so frequently used with differing connotations. In the Ilolt Duomarco terminology, collap c refers to any state of the van in which its crossectional area is not circular but his 45 uricd an elliptical configuration In ordinary usage 'collapse 18 often associated with a complete closure of the vein For greater precision the term partial collape is uscd herein for any state of a csscl 1 hich still per mits the pas age of fluid (lunbs of the curies in Fig 20 beyond zero) and 'com plcte collapse when it is flattend to uch a degree that no fluid pas es through it (point zero in Fig 20) Several problems concerning the effect of the venous pressure gradient on flow were studiсd in detail in our laboratory (Brecher 1952) This was done by cxamining phasic changes of low in the superior nu chia system of dogs with the cliest open All factors but one thic pressure gradient were held constant Tigure 23 shows a schematic diagram of the experiment The animals were in supine po stron with the external jugular veins and lieart on the same level ·00 VIVOLS KI TURY NuSory BOTTLE NGULAR VEIN P FEMORAL ARTEAY AICHT ATAN AR PESSURE CO FLOW FLOWMETER MANOMETER ES FIGURE 23 Faperimental arrangement for measuring drunage from superior can cau 1 Points O Sand I indicate where clamps are applied Clamp 3 is closed clamps 0 and I are opcoed for outdow met urement and simultancous compensation of right atral inflows CO = con tant pressure blood resen oir ES = escape vale Description in test The uperior cna c119 sus cannulated (P and C) permittin, flow cither througli 1 hunt Sto the riglit atrium or through an outflow tube // to acumulare fou meter of thic type shown in Fig 8 Reduction of the cardiac output throughe lo > of blood was presented by simultaneously infusing in cqux alent amount of blood into the right atrium from a low pressure reservoir CO Different pre cure gradients were applied to the cntire superior ciial s tom by sctting the outflow cannula at different levels and recording ouflou at cach lacl for 10 cconds The level of the outflow cinnuls ringed from 200 mm aborc to 600 mm belos the level of the jugular vein which is the reference or zero love Thi procedure allou cd flou mcisurment when the reins were other distended or as a re ult of suction collapscd in sarving degree Obviously the abrupt changes of the venous pre sure gradient ind mun tainance at 1 dcfinite level which were produced in these experiments do not occur physiologically This strictly controlled arran, cment wis lioncver nec essary for the investigation of the phyical factors determining venous flow dynamics Figure 24 shon a 6 records of a typical experiment demonstrating the relation bencen prcesure gradients and ena caval outflon * Figure 24A shows the effect of raising the outflon les cl from 0 to +60 min Pre sure measured in the citernal jugular vein rose steeply sathin two cconds from 39 to 68 mm is expected no flow occurred until a sufficient mount of blood hnd accumulated in the veins to raise jugular pre sure above the liciglit In this ap I all other experimeals reported from our laborators the pres utres were re corded with modified Gregg optical manometers For better repro luction the tracings in some of the orginal records from our laboratory have been renforce ·IEVOLS JIEMODI VAVICS 61 10 SEC- -10 SEC 88 68 40 40 39 WWW A +60mm 20cc 42cc Omm 35 36 66CC 63cc C -60mm D - 150mm 34 34 5 E -350mm Olcs F -550 mm 56cc FIGURE 21 Sex records illustrating the effect of the pressure gradient upon outflow from the superior carcas 25) tem Tracings from top to bottom in each record jugular pressure femoral arterial pressure bave line with time in seconds cumulative blood Don Calibration jugular pre ure in mom water fow in cc during 10 sec periods arterial pressuie in mm Hg with a range of 128/98 to 117/96 The high frequency oscillations in the fiow tracings of ricords L ind are due to spurts of blood setting the flow meter into vibration of thic outflou tube Thin flon commenccu lowly at first tlien at a fa ter rate (steeper lope) as jugular pre sure rosc gradually from 68 to 88 iom The total flow mounted to only 20 cc in 10 seconds Figure 248 illustrates the behavior of flow and venous pres ure when the outflow tube was at the jugular utrial levcl Venous pressure remuined constant before during and after mcasurcruent of flos indicating that during the outflow reriod re i tance to flor rounained unaltered Flow started immediately with the opening of the outflou tube and continued at an unchanged rate as cu drpced by the constant lope of the flow tricing The total flot nas 42 cc in 10 second Figure 240 lows thic cifcct of lowering the outflow level from 0 to -60 mm During the outflow period venous pressure fell steadily froin 36 to 12 mm of unter Flou began at a fa tiate and then decreased slightly Total fion amounted to 69 cc in 10 ccond Quite diffcrent results were obtained when suction was incrca ed from 0 to ·SHVOLS NITER сс -130 mm in shown into 240 Inous pres ure decreased within 35 conds from 36 to 6 mm of water and then lereld oli, never falling bxclou zero Flow started it a lugh rate but duerci id er wually Suddenly it I the steady flow topped moment irily and became pul itike is indicated by the watclic tricing Immedintely after the on ct of pul itione flow was greatly reduced The fic qucney of the pul itions x is not related to the heart rate Total flow during a 10 accond periol (63«) had not incru id in pite of the greater pre ure gri dient Records L incl F of F16 21 dupet the effects of further inerci c of uction In both can asteep fill of venous pro urt took place Flou commenced with Tirgi sush of blood then pulsations 1 chatter ) occurred due to the inter mittent coll up ing of the various s ulls Total flou amounted to 61 and J6cc ro pectively It appears from the c records that increase of suction results in 1 decre i of the rate of volume flow due to partial collap < of the icins The pres ure flou relitrons e tibli hed in this type of experiment are graph acalls presented in the 2) (data from another animal) In curie A flow in cc 10 see (ordinate to the right) is plotted against the pri ure gridient (mm water cis ?) between the external jugular pressure ind the love of thic outflow tubu above and below the level of the jugular von It is noted that when the level of the outflou tube is 120 mm above the jugular vein outflon is zero and the superior cava becomes engorged This congestion is back e indicated by the jugular vein pressurus (ordinate leítı bu fore the 10 sue flow period (curve B in 11g 25) and during outflow (curve C in rig 25) Durmb conge tion jugular enous pre sure to c from 39 mm to almo t 120 mm of water (pont not on Graph) When the outflow tube wis at the same level as the jugular sein out flon w is 44 cc in 10 seconds and the jugular pressuie remuncd practically unchanged (crossing of curves B and C) The largest flows (70 cc ) were obtained when the outflos tube was 100 mm below the level of the jugular icin Jugular pres uic then fell from 37 to 3 mm water Obviously up to tlus degree of suction flow increased proportionally to the pressure gradient without the intervention of collapse With greater degrees of cuction, blood flow fuled to inci case further and in fact decreased slihtly This is illustrated by the leveling and decline of the flox curve in lug 25 The fall of jugular scnous pres ure to zero indicates that outfion is limited by the advent of a partial collapse when the citra vascular pressure (atmospheric pressure) and intravascular pressure (zero right limb of curse C) reach an cquilibrium It is interesting that these pressure flos relations which cxit in the veins of lizing organisins (curse A Fig 25) have been established by Holt (1941) in experiments with physical models u ing collapsible rubber tubes and cicised cins From the floux records in lig 24 and flow pressure relations plotted in Fig 25 one must conclude that venous collapse docs not occur instantancou ly when the pressure in a downstream portion of the cssel is suddenly Ion cred Collapse is actually a two stage process The first is called the depleting stage (stcep flow increase in Fig 240) During this stage the transmural venous pressure declines ·TE VOUS TIEWODI NIMICS 03 and the vein empties most of its blood into the region of the lower pressure This 18 folloned by the collapsed stage of the vein which is reached after its depiction has been accomplished (sudden flon reduction in Fig 24E) From the data shown in Fig 21 it is non possiblo to calculate in ab oluto с +100- +50- B O o -70 A |-60 -50 x -40 30 -20 DE- CON- PLETING| GESTION STAGE COLLAPSED STAGE 10 0 +100 -100 -200 -300 --400 HIGC KE 25 Relation of flon and pressures in a collapsible system Cure A Flow pressure relation to drajnage from the superior vena cava trce Curse B Control sugular pressure before the 10 sec perio is of flow measurement Cure C Maximal riso (left lmb) or fall (uglt limb) of jugular Venous presure during flow measurement Note that in the collaj se! stage of the enous trec the pressure in the jugular sein never falls below zero le atmosplrric pres ure Ordinate for curve 4 (right) ce of vena cay al blood drained in 10 sec Ordinate for curves B and C (left) mom water Ibscissa for all cunes height of outflow level at one or I clow the lusel of the Jugular vein in mm water ·61 I EXOUS RCTURY 1500- DYN SEC COLLAPSED STAGE DEPLETING STAGE CM5 A 1000 500 CM SEC B 0 00 . LY NO 100 200 300 400 500 MM PRESSURE GRADIENT FI LUF G Relation of re tanre flow and pressure in a collapsible i ein of a hung dog The dat slow the relation of resistance (curve 1) to volume flow (curve B) during the depleting and the collap od stages of the superior vena cava system when different grocs of suction re applied to the end of the outflow drainage tube of the superior (nval vcin Ordinate for curi 1 (left) re i tance in dinc scc/cm Ordinate for curic B (night) Flow in or per re Ibscis for both curios pres are gradient between jugular con ani host of outflow Iciclo mm water unit the reast ince in the sons at different degrees of uction using the formula Q: Pi - P2 R The results irc graphicalls represented in F16 26 Curic I shows that the re sistance did not change appreciably while outflow from thic vein (curve B) in creased upon moderate suction such as one can observe during the depleting stage How cvcr 19 oon as the collap ed stage of the cin was reached re sistance to flow increascd progressnicks with greater degrees of suction Atten tion is called to the sudden brcah in the cour c of the two curies which clearly illustrates the different behavior of the reins in the two tages The experiments in living animals revealed the inportance of the time factor for the des clopment of collapc25 maniſested by the custcnce of the depleting stage It was of intuie t to (e uliether thic depicting stage was also reproducible in physical analogue Collap ible rubber tubing was u od to represent a sein Flow was recorded in a manner corresponding to thint in tlic inimal experiments Figure 27 illustrates the flow pressure re istance relation in a collap ible rubber tube In the rubber segment undergoing deplction resı tance to fon semained nearly constant (horizontal part of cure A) whereas for varied linciriz with the pressure gradient (ascending limb of curve B) Horcyer, as soon as the suetion was increased sufficiently to cause the rubber tube to enter the col lapsed stage (at about – 70 mm suction) resistance increased progressively (ascending limb of curre 1) vereis flow remuned constant (horizontal part of curve B) Comparison of the pre sure flor resistance relationship in Figs 26 and 27 ·VEVOUS MIESTODI VANICS Ou COLLAPSED STAGE 6000 DEPLE DYN SEC TING CM5 STAGE 4000- 2000- см2 B SEC 8 20.000.000 0 100 200 300 400 MM PRESSURE GRADIENT FIGURE 27 Relation of re istance flow and pressure in a collapsił le rubber tube which is ar rang d in physical model so that it corresponds to a vein in a living animal Plotting and labeling, are the same as in Fig 26 except that a collapsible rubber tube replaces the perior vena cava u reveals a remarhable similarity of flow behavior of vcins in situ and of the collapsible tube of the plıysical model This emphasizes the purely phyical nature of hemodynamic cients in senous collap e Summar ing Increase in the pressure gradient along a collap ible ven by the application of suction at one end re ults first in the emptying of the st el (depleting stage) before at enters the collap ed stage During the depleting stage outflow from the vain varics in proportion to the pressure gradient and resistance to flow remains approximately constant During the collap cd stage outflon from the vein re main approumately constant while the re i tance becomes greater with an incrca c in pressure gradient SIT\IFICAVCE OF Evous COLI APŠE IN THE PERII 11ER AL CIRCULATION The fundamnental flos dynamics in collapsible tructures may help to ex plain venous flow in various physiological conditions Some of these con idera tions arı not ba td on direct caperimental evidence and require further experi mentation Locall leveloped flox pul ations as shown in records D E and F of Fig 24 are not neccs anly characteristic of venous bchavior in the collapsed stage The pulations cau ed by a momentary complete collap e of a venous egment in which intraluminar pre sure is excccded bs cxtraluininar pressure The blood ·66 ILOLS RETURN uluch continues to flow from the capillaries into the peripheral portion of the icin forces the closed segment to open again The following complex relations of frequency and amplitude of the pulsa tions were found in living animals and play sıcıl analogues (Brocher, 1902) The frequency bccinc lugher with (1) Incrcasing rigidity of the res cl wall ind surrounding tissucs (2) a decrease of volumc fox through the vessel and (3) grcntcr suction The amplitude became greater with (1) a decrease in fre quency (2) greater volume flow and (3) less suction Pulsatilc flon is often reflected in oscillations of 1 cnous pressure not related to the heart rate Pulsa tions of a frequency as low as 1 per 20 seconds and as high as a few hundred per "cond could be produced in suitable analoguls In animals sc have re corded pulsations ranging in frequency from 3 to 20 per second Pulsations in collap cd reins do not occur so often under physiological con ditions as they do in cxperimental systems where a collapsible tube 18 cıpanded by a rigid out fou cannula lnder normal conditions, in man and animals, pulsations can be occasionally observed at places where a collapsible vein cnters a los prc sure region through tissues which tend to keep the vein open such is the entry of the thoracic cage On the basi of this knowledge an explanation can now be ndvanced for the behavior of jugular scnous flow which Barrs (1821) ob crued in a standing hore (19) Obuously flow through the glas, bulb cannula in crted into the jugular cın can not be augmented by inspiration bccausc under Barry s par ticular cyperimental condition (collapsed stage of vein) flon would not increase with greater suction (right limb of curve A in Fig 24) Thc pulsatile flow in the glass bulb sas merely the result of local pulsatile collapse of the vein in dependent from the heart action (comparc Fig 24) Vany veins are unitomically so situated that they collapse casily when the extravascular pressure exceeds the intravascular pressure For surface seine the most important cxtravascular pressure luich leads to collape is the at mospheric pres ure in deeper veins it is the surrounding tissun pressure acting on the venous walls However it must be borne in mind that not all seins are collapsible This applies particularly to the venous sinuscs such upon suction are held open by the counterforce of firm walled tissues such as exist in the skull bones Iiver and spleen As long as the volume of cerebrospinal fluid remains constant the venous plexuses cxtending the whole length of the spinal column and the intervertebral veins serve as an incollapsible communication system for the return flow of blood Via capillaries and venous ainuses in the skull these icins form a communicating system with the arteries corresponding to an inserted U tube in 3 person sitting or standing up Flow through thus U tube system would not be much affected by positional changes (sce also Fig 3A) Oxing to this rigid communicating system subatmo pheric pressures can develop in the cerebral sinuscs during head to foot (positive) acceleration on a centrifuge without much impairment of the cerebral circulation (Ru hmer et al 1947) One may therefore state that venous return in head, nech and trunk occurs over two principal routes through the incollapsible skull and crtebral channels and through collapsible seins Both systems communicate at all les cls Iittle ·VENOUS HEMODINAMICS 67 is known about the flon interrelations of the two routes It appears that, re gardless of positional changes flow from the head remains relatively constant owing to the flow dynamics peculiar to each system That is flow through the rigid vertebral system does not change by virtue of the Ushaped communica tion with the thich walled arteries (see Fig 3A) and flow in the collapsible system remains constant due to the resistance changes in the partially col lapsed veins (see behavior of flow and resistance in the collapsed stage Fig 26) Parenthetically it should be mentioned that the giraffe and the human being do not differ essentially in their problems of cerebral blood supply This subject has always fascinated physiologists and lay men as shown by the wide interest given the attempt at measuring the giraffe & blood pressure by Goetz and Budtz Olsen (1955) and Goetz (1995a b) Flox to and from the giraffe s head in the erect position appears to be assured by the siphoning action of the rigid com munication system of arteries and intervertebral venous channels Even if the pressure in the cerebral sinus were subatmospheric return flow through other icnous channels would be automatically regulated by the collapse mechanism With the giraffes head los ered the rigid siphoning system would not es sentially change However when the head is lowered the collapsible nech veins would become greatly distended by a high hydrostatic blood column This is apparently presented by breaking up the high column into small segments since the jugular vein of the giraffe contains numerous valves as Goetz has shown Summar ing Pulsatile flow through collapsed veins occurs under certain normal and ex perimental conditions As a local phenomenon it is unrelated to pulses origi nating from the heart Venous return in head neck and trunk occurs via two routes (a) through a system of collapsible veins and (b) through a system of incollapsible veins in the cranum and vertebral column The latter acts to gether with the arteries as a siphon through which blood flor becomes rather independent of changes in position THE VIUSCLE POVP WITHOUT VALVES The effects of contraction of voluntary muscles on venous return have been amply studied and reviewed (Ledderhose 1906 Jager 1937 Franklin 1937 Burch 1950) One may conclude that provided all other factors (arterial per fusion pressure etc ) remain the same venous return is increased by the me chanical action of muscular contraction in the reins The presence of venous valves has often been considered as being of prime importance in assuring effective movement of blood toward the heart during the milking action of the muscle pump However anatomical vals es may not be essential for this Alexander (1931) stated concisely the basic issue Extra vascular compression of a ve sel will result in an equivalent flow of blood in both directions from the point of compression only under the conditions that the re sistance to flow in both directions is the same If there is a difference in the re Bistance in the two alternate directions then greater flon wall occur preferentially toward the end of least resistance Even in the complete absence of ana ·68 SEXOLS RETUR tomical 1 alics the sesscls tos irds the capillary end of the venous system to.cther with the continuous arterial inflou should always represent a big nificantly greater resistance than that found in the casels ton ards the heart together with the cardize outflon In view of this relationship rhythmical compusion of any ten should aid in propelling blood bach towards the heart' roi clarification it may be added that these considerations do not conflict with the fact that the central function of the venous values is to present over distension of the venous u ulls in the dipendent parts of the body (ce page 19) The phy iological and pathological importance of this problem necd not be implified Vlint eins do not contain valves, ce scins within the muscles The likes are lucated at the cut of the ein from the muscle In adı inced age and under pathological condition alvcs may become incompetent or dis appear Neverthel it is often ob cried clinicalls that ccn in the absence of als nous return improve during periods of rhythmical muscle more ment in connection with the studies on cous collapse our laboratory group became intere ted in the search for i mechanism which could promote venous return through vilseless suns (Brecher et al 1992) In order to accompli h tl all factors which in an experiment could alter cnous flow uch as chinge of arterial inflow humoral metabolic and nervous influence had to remain con tant Thus the problem became a purely mechani cal one which c in be inted in its basic forin Docs rapid rhythmical compres ion (collapse) of von augment the rate of volume flow through it? As far is the mechanism is concerned it is immaterial what catrazecular force chu (s the collapse of the vein (eg compression by ur or muscle liga mont joint bone cte ! For cyperiniental purposes venous collapse was brought about by atmo pheric pressure when suction was applied to a venous outflow tube using an arrangement similar to the one illustrated in Fig 33 It was de termined thether or not frequently repeated depletion and refilling of the veins by rapidly alternating pressure gradients results in net increase of flout otcr that obtained when the same pre sure gradients are less frequently acting Under these strictly controlled conditions all factors remained the same except for one variable the frequency with #luch seins were compres ed The experiments in living animals were duplicated by plus sical analogues in which collapsible rubber tubos nere used instead of veins In Fig 28 four records are shown demon trating the effect of the alternation between two pressure gradients on volume flow through collapsible structures during a 12 second flon period Records 1 and B arc from experiments on a physical model using rubber tubing records and D are from a dog In the records on the left side the stoeper of the two preesur gredients (350 mm water) acted for 6 seconds bringing about depletion and partial collapse (1 to 1) This was follon cd by the smaller pre sure (40 inm water) acting for 6 acconds (1 to Z) such resulted in outfloss without collapse of rein or rubber tubing On the right side outflow and pressurca u cre recorded when the simc two pressure gradients (1 to Y and I to Z) were alternated cery tso scconds In the physical model, flow is inercased from 103 to 115 cc (11 6 per cent) simply by alternating the to pressure gradients every two seconds In the cor responding dog cyperiment enous drainage from the superior cna cara nas ·103 cc FLOW 115cc FLOW 50 PRESSURE IN -O COLLAPSIBLE TUBE Х Z -12 SEC -12 SEC 150 ARTERIAL PRESSURE -50 110cc FLOW TIIE RESPIRATORY PUMP 95 cc FLOW VNN X FIGLRE 2$ Illustration of a net flow increase by the frequent alternation of pre ure grn lients in cins or collaj ible tubes A and B = 1ccords froin physical models Tracings fion for to bottom cumulac flor pressure in collap ble tube bise -50 JUG VENOUS LO PRESSURE Y Z line C and D = records from dog Tracings from top to bot tom bare line femorul utery preure cumulatise flow jugu lir sun pre sure at junction of external maxilluy and facial ein 69 ·70 ZVOLY RETUR incre dued from to 110 cc (137 per cunt) by the same mancuicr This cy permout could be continued for much longer periods than 12 acconds The net incrcase of total flow by the frequent alternation of the pressure gradients is due to the fact that in the collapsible structure a re crve of flud accumulates during each incidence of the smaller pressure gradient (muscle relaxation) Then since resistance to flow in the collapsible segment is shall low duning the depleting stage, a large volume flow occurs when the sein begins to empts under the influence of the high pressure gradient (muscle contraction) Is soon as it is emptied and the collap ed stage is reached, resistance rises sharply and the flow rate drops a siruple calculation from the records in Fig 27 stions that the mean resistance in the cous trce nas decreased during the 12 «ccond flon period from 2414 to 2082 dyncs scc/cm (138 per cent) merely by alternating the pris ure gradient more frequently The implications of the c esperiments are obvious Thcy establish the cust enec of 7 imple phrac il mceliani m by which one can explain an augmentation of cnous return in ılıcle s vesels through rapid rhythmically alternating movements such as occurs in walhing running clercising etc Summanzing Rapidly alternating compressions of collap ible vals ele cins increase flow compared with that occurring with le s frequent compressions ·VII The Respiratory Pump An understanding of the collapse mechanism has greatly arded in approaching the cardinal question Does inspiration augment venous return or not? (See pages 8 and 27 ) TIME Factor I VEXOLS COLLAPSE In the outflow experiments shown in Fig 24 the sudden suction exerted on the superior vena cha would physically correspond to the suction on the extra thoracic eins exerted by an inspiration in an organı m with the chest closed It hould be noted that the collapse of the reins by suction does not occur instantaneously with the onset of aspiration The records in Fig 24 illustrate that collapse 18 not only a function of the magnitude of the pressure gradient (suction) but also of the time over which acts This is graphically represented in Fig 29 by plotting the time it takes the reins to become depleted against the degree of suction (pressure gradient) The data are taken from the records in Fig 24 and other records from the same experiment According to these measurements the duration of the depleting stage lasted 35 seconds at a suction of 150 nm mater At greater aspiration this time became progressively shorter From the findings in the e strictly controlled open chest experiments one can predict the effeut of inspiration on venous return in the closed chest Under phy hological conditions in the recumbent position with the venous bed at the hydrostatic level of the heart quiet inspiration may merely be expected to deplete the peripheral veiny without inducing their collapsed tage The suction would be too little and the time over which it acts too short to collapse the extrathoracic reins For illustration 3 typical intrathoracic pre sure curve (Fig 29 curse B) of a quict spontaneous respiration is entered on the graph Onks forced deep inspirations would produce negative pressures of sufficient magnitude and duration to bring about the collapsed stage This is illustrated by the intrathoracic pressure curve (Fig 29C) of a forced inspiration (Muller : experiment) The next step is to prove that this is the case Summarı ing From venous drainage experiments it is predicted that in piration should augment venous return by depleting the blood from the extrathoracic veins into the thoracic veins During quiet inspiration in the recumbent position the extra thoracic veins should not collapse to such an extent as to throttle venous re turn During deep and prolonged inspiration the extrathoracic veins should after their depletion enter the collapsed stage and prevent a further aug mentation of Venous return EFFECT OF RESPIRATORY VIOIEVENTS OY SUPERIOR CATAL FLOW In this experiment a Pitotmcter (Fig 11B) was inserted into the superior certa car a of a supine dog Then the chest was closed and normal intrathoracic 11 ·72 TE VOUS RETURA pressures were ic established (Breciicr and Vixter, 1903) In contrast to the cumulatıc (slope) records shown in Figs 21 and 28 this device indicated the rate of volume flon (sce page 30) Figure 30 shows a segment of an original record illustrating the cffect of normal quict breathing on scnous return Ilox measured at comparable phases of the cardiac cycle, incrca cd from 52 cc /sco during the respiratory pause to 11 cc/sec during inspiration hight atrial pres sure declined in the usual manner with the lowering of intrathoracic pressure Jugular pressure measured 7 cm ceplinind to the first rib, fell from 35 mm water to zero lion thcsc findings one mu t conclude that venous return in crcices significantly with inspiration Larmination of the flow tracing ml 18 30 rctcals that during quict in piration inflow into tlic right heart, as predicted is not throttled by a collap c of the cins at their entry into the chost To scc whether a decp and long in piration would brmg about the collapscd stage in the predicted manner, flow was meas ured during partul occlusion of the trachca during the scry ncıt inspiration following the quict in pıration slios n in Fig 30 The tlon occurring during this forced inspiratory attempt is illustrated in I g 31 IIcrc agun inflow increa ed immediately at the onsct of inspiration In fact it increased more rapidly and to a greater citent (135 cc /sec ) as the fall of intrathoracic pressure de vcloped more rapidls and to 3 greater depth than during quict inspiration However after 1 to 2 cconds flou diminished in spite of continued inspiration The decicise in flow occurred although right atrial pressure declined further and the pres ure grudiunt from tho jugular vein to the right atrium bocume grcator Obviously a resistance to fou developed between the two points of pre uro measurement (jugular vein and right atrium) because the extrathoracic veins entered the collapscd stage Evidence for the occurrence of a partial collapse of the extrathoracic veins near the entry of the chest is seen in the course of tho jugular ous pressure It began to fall sath the onset of inspiration and finally reached zero but did not develop a negative pre sure Then shortly after having reached zero at began to rise again although the thoracic a pration was still increasing This peripheral venous pressure rise must be caused by the combined action of a lugh 10 istance in the partially collapsed vcnous egment near the entry into the thoracic cage and the continued inflow of blood froin the capillarics Since the jugular pressure rise from zero commences imultaneou ly with the end of further ineren of flow the corrclation of preacuic flow and resistance in the collapsed stage becoincs very apprrent It is basically of the same nature as that produced under the strictly controlled conditions in luch venous collapse had been studied previously The correlation of the pressure and flon tracings in Fig 31 demonstrates that in the zenous system flow does not necessarily increase proportionally to an increase in the pressure gradient From these experiments it becomes apparent that the two control ersial cus the classical aspiration" and the collapse thcors of venous return do not conflict but actually complement one another Venous collapse during inspira tion docs not occur instantaneously but is a tu o stage process During the first ·DE PLETING STAGE COLLAPSED STAGEN TIL RESPIRATORI PUMP 73 stage the depleting stage, the demands of the classical theory are satisfied Venous return to the heart varies in direct proportion to the prescure gradient During the second stage the collapsed stage the collapse theory of Holt and Duomarco is applicable venous return is not augmented because resistance increases with greater pre suri pridients Previous farlure to recognize this situation must be a cribed to the fact that only the simultaneous direct ri cording of plasir changes in fios and pressure with instruments of adequate sensitivity and frequency re por se could furnish the necessary information It remains to be demonstrated that the yugmentation of venous return dur ing inspiration is not cancelled by a corre ponding Now reduction during en piration or in other words that the respiratory pump provides t net gain of 0 -1001 IC -2004 0 - 300- -400 --500 M -600- 3 SEC FIGURE 29 Relation of the duration of the depleting and opset of the collapsed stage to the degree of suction appled to the superior yen3 myal System Cune duration of cou3 depleting stage et dfferent degrees of aspiration Curse B typ cal intrathoriek pressure during quet respiration Cun0 C typical intrathoracic pressure during Nuts espera mcat Ordinate o galite pressure in an ater

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·150 ART 100 0 ATR -230 -150 FLOW 135 cc 12 CC TIIE RESPIRATORI PUMP 50 JUG VEIN 52 CCS 0 FIGURE 31 Lffect of diep ind prolonged spontaneous r piration (Muller sey erimcnt) on icnous return in the cloud che t Tiacings 1 in Ligure 30 70 ·76 VEVOUS RETURY Icnous return This problem has long been known Tolkmann (1830) mentioned that if in piration did increase icnous return cxpiration might decrease it by the same amount Crimination of the records in Tag 30 and 31 rcicals that cnous return is slightly reduced upon cypiration since the pres ure gradient is loss and the blood rescrvoir in the extrathoracic scins requires time for re pluushment Honcier, the capirogenic flok reduction is not so great as the inapirogene ugmentation is a result thert 14 å net gain of return flow of blood to the heart by the action of re piration The physical principle of the underlying mechanism s bich mcrcases the net repous return by the rhythmical action of re prition is in ca ence the same as that illustrated in Fig 28 In tho cuyperiment it u is dainon trated by ducet mcisurements that rhythmical depleting ind refilling of the peripheral cins may incrca c nct scnous return Eck tein et al (1917) ob cried in dogs with open chest an increasc of in fonor zena cara fou when the diaplıram mu cle contracted Such flow aug Izentation was obviou ly not causcd by thoracic aspir ition but by squeezing out of blood from the abdominal inferior caval trec To determine whcther contrictions of re piratory muscles affect flos also in the superor yanı caval tributario ne ma ured upcrior casal flow in the open chit This was done in order to ( tablish whether the respirator flow increa c boxn in Figs 30 and 31 is actually due to thoracic aspiration (suction) or to a squcczing out of blood from Citrathoracic cins olcs by respiratory mu cle contractions (Brocher und Vater 1933) The record depicted in Fig 32 was taken when artificial reparation w 13 di continued for a brief period and spontaneous ro spiratory movements reappeared Onset and duration of a forceful inspiratory attempt is indicated by the tracing from a pncumograph placed around the open chest The flow tracing remained c sentially unchanged during apnca and during the in pirator cffort From thus caperiment it can be concluded that the contractions of the respiratory muscks per sc do not augment flow in the su perior cival istem The incre 1 c of superior car al venous return in the clo ed chest must thcrcfore be attributed to thoracic aspiration Summar ing In the clo ed chest spontançous respiration augments venous return in the superior vena cara The increase is caused by emptying of blood from the extra thoracic veins (depleting taget into the thoracic cins After their emptying the extrathoracic cids enter the collapsed tige of the in piration is deep and long in the absence of thoracic aspiration (open chest) superior casal flow remains con tant when re piratory iu cles contract IVLIENCE OF RESPIRATION ON I\FERIOR CALAL FLOW The Ituation in the inferior cna cava is more complex than in the superior caval tree Whereas the superior caval system traver cs es cntially tro com partments of changing pres urcs (thoracic and cxtrathoracic areas), part of the inferior cura druns through three compartments (thoracic abdominal and cxtra abdominal areas) In the inferior caval s tem pre sures muy vary in dependent) according to various actus itics of the body For cuample, during

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·78 TEVOUS NETUR spontinous inspn stion intrathoracie pre urt decline intra abdominal pres sures ri e, and the tissue pressure level in the legs remains unchanged Special anatonucal structures such 18 the caval band' at the les el of the diaphragni (described and emphasized by Franklin and Janber, 1934, 1936) may hinder flow from the abdominal to the thoracic inferior cua during inspiration for an underst inding of the over all behavior it is therefore necessary to consider the various factors aside from thoracic . piration which are operative in de termining return flow in the infcrior scha cay. This was done by Vrater (1933) in our laboratory With two Pitotmeters (Hg 11B) Vater directly compared flows in the tho racic and the abdominal portions of the inferior vena cava the latter being measured below the renal veins rig 33 shoss 1 section of flow and prescurc tracings taken during natural respiration of a closed chest dog The fox curves from both the thoracic (VC 1) and the abdominal (VC-2) portion of the caval vain show cardiac variations details of which will be considered later Thoracic AO 150- AD -0 1004 50- 50 O- E-100 30 VC-! 150 20- 200 YC 2 20- my 10 ус mm Wher wowin mann ww 0- 10- VC-2 IA O- -100 0 10 -50- 90 -100 RA 607 -1501 BO 50 - 200 FV 70 40- RA -60 IA FV 50 10 20 30 SECONDS FIGURE 33 Effect of natural breathing on flow a the thoracic and abdominal infcrior na cara Tracings from top to bottom aortic pressure (40) in mm Hg intrathoracic i resaure (IT) in om water thoracie inferior cara blood flow (1C1) in cc / cc ab lominal inferior pena cay 1 blood flow (102) in cc /sec nght atrial presure (R1) fenior il vein presur (IT) and intra abdominal pres ure in watcr Time in second (lfter Vater 1903 molific I fiomn original) 30- ·THE RESPIRATORY PLUP 79 flow increased during inspiration with retention of the cardiac variations but the general flow lusel changed much less in the abdominal cara and the cardiac Variations became almost obliterated as at D and E The latter phenomenon ocurring synchronously with the leveling off of the rising thoracic flow curve appeared to be caused by the onset of the collapsed stage analogous to that described in the superior casal sy stem It is further noted that with the descent of intrathoracic and n_ht atrial pressure intra abdominal pressure rose This in itself would aid in the cmptying and collapse of the abdominal vena cava Femoral venous pressure rose slightly during the deeper (first) inspiration apparently owing to the re istance increase in the partially collapsed inferior cava In order to eliminate the contribution of the diaphragmatic contraction to the inspiratory flow increase and to see whether thoracic suction alone would augment inferior caval flox Mixter quickly cut both phrenic nerves in the closed chest while taking a continuous record Figure 31A shows a segment of the record during pontaneous quiet breathing illustrating the concerted action of intercostal and diaphragmatic muscles Segment B was taken briefly after the phrenicotomy, when respiration was maintained by the intercostal muscles only Segment A shons an increase of thoracic inferior caval flos at the beginning of inspiration then a leveling off when the collapsed stage was reached Abdominal caval flow dininished throughout the in piration This diminution was caused by the partial collapse of the vein due to the abdominal pressure rise The partial collapse of the abdominal can leads in turn to a slight rise of femoral venous pressure After phrcnicotomy (B) intra abdominal pressure (GA) fell during inspiration femoral venous pressure (FV) declined slightly abdominal caval flow increasnd slightly but distincth and intrathoracic caval flor increased throughout inspiration The average thoracic inferior Caval fons before and after phrenicotomy were not significantly different These experiments demonstrate (1) that thoracic suction alone can augment inferior caval flow and (2) that the diaphragmatic contraction squeezes blood from the abdominal cava but in doing o enhances the partial collapse of the abdominal cava wlien it is comprc .cd by the abdominal contents These findings do not support the idea of a diaphragmatic sphincter advanced by Franklin and Janker (1934 1936) and Franklin (1937) Such a sphincter would prevent the inspiratory flow augmentation The various factors affccting flow through the inferior caval system dur ing different types of respiration are quantitatively represented in Fig 30 (Mixter 1993) For better visualization the flow during each cardiac cycle as integrated and then plotted In cach plot the upper curse represents flow in the thoracic cay and the lon er curve shows the flow in the abdominal cava below the renal veins It should be apparent that the thoracic flow is greater than the abdominal flow by the annount contributed from the renal and portal outflows The dotted lines symbolize mean flows throughout the respira tory cycle For comparison thoracic casal mean flow mas maintained in all re piratory conditions at about the same level through judicious blood infusion The floty duta in Fig 35A show the constancy of flos during apnea i eta in the open chet ·SO (A B AO 150 too- VC1 50 X 50 40- 50 O IT 30- -100 VC 2 20- Anh who 15 VCI 10-1 150 10 -101 5- 0 VC-2 O IA 100 FV RA 60- -50- -90 50- -80 404 100- sol RA FV 70 L60 20 0 10 FIGURC 34 Cliect of acute licnicotomy on inferior casal flow in the clo cd chet Tracinge in una nt brenneries in tact Segment B 1 minute allir nere scelion Role er ist ence of cuatryctal acceleration (1C1) csen though abdominal 50 60 70 te ure falls during in pration \blominal flows (1C2) are nox au cel til during this l is rather than sctardo (com pire with 1) (liler Muxter 1933 modifical from original) ·TIIE RESPIRATORY PUP 81 30 30 20 20- as 32 VC 32 22 o C2 76 0 O SEC + 0 SEC → o ina 13 9 0- 36 SEC SEC FIGURE 35 Flow through the inferior caval system as influçaced by certain re piratory com ponents Sold lines mean flow per cardiac cicle through thoracic cava (1C1) and ab dominal cava (VC2) Dotted lines mean over all flow during period analyzed and I = onset and cessation respectively of inspiratory phase of respiration 4 = flow during hyperventilation apnea che open B = depression of flow during positro pressure in fation of lungs che t open C = effects of diaphragm de cent che t open D = flow behavior after chest closed Figures at right hand end of charts refer to values for over all mean flow in cc /sec (After Mixter 195 ) In 35B a positive pressure lun, inflation beginning at 1 and cnding at I re ulted in a flor reduction in both portions of the cava In 3.C the effect of respiratory attempts in the open chest is visualized Intra abdominal pres ure began to rise at 1 (onset of in piratory effort) leading to a thoracic caval flow increase and an abdominal caval flow decrease The reverse took place when it began to fall at I end of inspiratory effort) In 35D the chest was closed I and I denoting the onset and cessation of spontaneous inspiration respec tively Thoracic caval flon was greatly increased during inspiration and de presscd during expiration hereas abdominal caval for became practically constant This shows that flow through the abdominal cava is most efficiently main tained by the combined action of thoracic suction and abdominal compres non nilich balance one another rather delicately of the four respiratory conditions shown in Figure 33 mcan fou in the abdominal cava was greatest in the closed chest (35D) All studies on senous collapse mentioned so far weic undertaken on animals with normal hlood volume Honeycr one could well imagine that the depleting ·S2 IFVOUS RETURN 257 20- 5 GC/SEC AO B 10 5 INSPIRATION B 0 -10 -05 0 05 LO 15 20 25 SECONDS FIGURE 36 Lirect of venous plethora upon in piratory augmentation of thoracic inferior cual flow Ibscis time 10 seconds Ordinate blood flow in cc /sec Animal progres. cly tran fused between curse 1 (mean blood pressure "8 mm Hg) and cunc D (mcan blood pres sure 129 mm Hg) il re piratory cscles of samc leogth lote progressi els fuigher banal levels proges. n cls greater maximal flows and progi essisels prolonged increase of volume flon luring in.piration (w and z) (After Muxter 1933 ) stage would be shortencd in a hy posoleme anım il s hose catrathoracic venous 16 crvor would be quickly emptied with the onset of thoracic a piration The modifications of inferior caval fou by liy povolemia and hypervolumia were stud ied by Vrtor (1933) during spontaneous respiration in the closed chest Figure 30 13 1 composite graph of inferior caval flows taken during four respiratory cycles of the same length and depth in the same dog Between the first respira tory cycle (1) and the last one (B) the animal was transfused until the mean arterial pro surt rose from 78 to 122 mm Hg While the basal flow during the expiratori puu e became somewhat greater with mcreasing picthora of the cava the mot striking feature was the progressive increase in the maximal flows induccd by inspiration and the concomitant prolongation of the depleting stage before the onset of the collapsed stage (Il II and 2) is reached Summarizing In piration causes a inificant augmentation of venous return va the in fenor rcna cara Two forces are commonly invols cd abdominal compression and thoracic suction These forces ordinarily upplement one another but eitlier onc is capable of acting separately The forces governing cxtrathoracic venous collapse obtain also in the infcrior cava The clevation of abdoininal pressure enliances thic tendency toward collap c ·CIL RESPIRATORI PLY RESPIRATOR) ARIATIONS OF PORTAL FLOR It ha bccp cu.ge ted that among the abdominal organs the liver may con tnbute pecifically to an augnientation of inferior caval flow duriog nspiration (For revien see Gollnitzer Vicier 1932) Bs nicasuring Urainage from the portal vein through an outflow cannula Alexander (1931) demonstrated that the contracting diaphragm compresses the hepatic and splanchnic beds und muy thereby increase venous return when he used the drainage method the resit ance of outflow froin the portal bed rem uncd constant because the outfiov cannuli basket at a fixed level during the flon determinations Hotcuer such a situation may not prevail when the portal circulation remains uninterrupted between the planchpic area and the liver vascular bed With the continuous circulation the resistance to flow from the portal vein into the liver may be altered when the liver is compressed or shiſted by tlie contraction of the dia phragm As part of a recent study op lncr flow we re examined this problem in our laboratory by inserting directly into the portal vein a bristic flowmeter (Selkurt and Brecher 1936) The flow measurements were undertaken in Daturally breathing anesthetized dogs In this experimental arrangement part.sl flow would be affected not only by a compression of the splanchnic bed but al o by resist ance changes in the laser bed that might occur during respiratory movements As illustrated in Fig 37 portal venous flor (second curse from top) decreased slightly but distinctly during inspiration Simultaneously rcuorded portal K { SEC - +200 360 -+150 CC/MIN 240 0 -100 Lioo INSPIRATION FIGURE 37 Changes of portal venous for Juning natural breathing Tracings from top to bottom portal venous pressure 9 mm water blood flow in portal sein in cc/min hepatic Tencus pressure in om water intrathoraric pressure during onc tespirator cicle (Unpub hcr ar 1 of Srihurt and Brecher) ·81 ICVOUS RETUR venous pressuri rose, wherca, hepatic icnous pre uie declined with the greater negativity of the intrathor.cic pressure This pattern of portal flow behavior was general in these caperiments Ilthough it mit sem otcryle at first glance, the c results do not conflict with the previons findings of Alcxander (1951) The dipinishing of portal flow in our experiments evidently resulted from an increase in rc i tance to blood flow through the liver bed when this organ sas compressed by thi descent of the diaphragna This capi ination is supported by the fact that the pres ure gradient along the vascular bell of the liver from the portal to the hepatic icin become greater during inspiration Thus it appears that in piration has a dual effect on portal venous flow dynamics By compreasing the splanchnic bed flow tonard the lıser is augmented (Alexander 1901) However on ing to a concomitant increase of resistance in the lucr bed thus increascd volume flow is not pas cd on to the liver icin. Instead at leads to a sliglit pooling in the portal ein s here flos 18 sloned down during inspiration The pooled portal venous blood would then be nulable for filling of the vascular bed of the liver during expiration On the other hand it appears safe to assume that the compre sion of the Incr during inspiration re ults in a simultancous emptying of the hepatic 1 enous channels toward the inferior vena cal Summar ing Flow in the portal sein decreases slightly during inspiration oking to a re sastancc increise in the vascular bed of the liver Hoxcier hepatic scnou flow may incica e during inspiration RESI IROGENIC CILATGES OF TOT IL VEYOUS RETURY After 1 separate treatment of each vena cava sy stem it appeared nece ary to cstablish the synchronicity and interrelation of the flow events w both ve lis Flow w is simultaneously measured in the superior and intenor vena raia with two Pitotmcturs (Brecher and Vater 1932) or two bristle flow meters (Hubay and Brocher unpublished) Theie ults are shown in Fig 38 Both segments were taken from the same record The trucings in the left segment of Figure 38 cre recorded during spon taneous respiration with the chest closed It is noted that flow increased and decrca od synchronously in botlı 071 n during the cardiac and respiratory cycle Intra abdominal pressure (dotted in the record) and femoral pres ure ro e dur ing cach in piration In the left segment fons and pressures were recorded 17 seconds later after a quick thoracotomy when the animal made re piratory cfforts The strong diaphragmatic contractions produced higlier intra abdominal and femoral pressures In the absence of thoracic suction, infcrjor car al flow s as distinctly elevated as a result of the squeczing out of blood from the abdominal inferior caval tree (see also Echstein et al, 1917) Superior cual flon 18 practically unchanged These findings tic together the individual obsert ations shown in Fig 30 to 34 Thus under natural conditions thoracie a piration affects venous return from the upper and lower parts of the body in like manner and leads to an augmentation of right atrial inflox via both casal seins ·TIIE RESPIRATORI PUMP 8) CC/SEC C/SEC 30 -UP VA INF CAVA 30 -20 20- 10 0 roo 100 -Rot FEM VEIN 100- محمد 50 | SEC 0 2 SEC CLOSED CHEST OPEN CHEST FIGURE 38 Effect of respiration on total venous return measured simultaneou ly in the supe rior and inferior vena cava Left segment Spontancous respiration with chest (lowed Right Begment Re piratory movements during open thoracotomy Tracings from top to bottom aortic pressure thoracic inferior caval flow in cc /sec superior ca al flow in cr / sec Intra thoracic pre sure in left segment forms an undulating line and in right segment (after open ing of chest) a traight line ag atmo pteric zero pressure below the cortic pressure tracings Right atrial pressure femoral venous pres ure in mm wuter Intra atvlominal pressure dotted in rccord for better visualization (unubhashed recorl of Vister and Brecher) Suminar iny Re piration augments synchronously total venous return from both casal veins under normal conditions REGION OF VENUS COLLAPSE DURING ISPIRATIOY Even though it has becn demonstrated above that collapse does not occur instantancou ly at the onsct of inspiration and that at least a portion of the cxtrathoracic venous reservoir is available for depletion into the thoracic veins little is known about the scgment of the vein which collapses Specifically it should be determined hcther as Duomarco (1941) claims the veins collap e at a harply demarcated point at the thoracic inlet or whether longer segments of the extrathoracic vessels collapse Since a partially collapsed portion of a vessel offers an increased resistance ·86 VI VOUS RLTIRI INYAATHOA cic MANOMETER GULAR VEIN RIGHY ATRIU A EXPLORING CANNULA INFUSION FAM FEMORAL ARTERY FROM TF CONSTANT PRESSURE RESERVOJA DIFFERENTIAL MANOMCTER VENTURI METER TIGER 39 I xperimental arrangement for studying the regional cffects of venous collat BCD00E = route of blood flow from external sugular vein to exploring cannula FC CD and I = route of infusion fund from constant preasure reservoir through intuisi ter to cxploring anuli Tubing can I c clamped at 1 lor B for sinon Touring of sow De scription in text to infton this plenomenon was utilized for an exploration of the onset duration and extent of collapse in different regions of catrathoracic veins during normal re piration (Brecher et al 1952) Figure 39 shows a schematic diagram of the experimental arrangement Infiou from a constant pressure reservoir "1s recorded with a venturimctor us an exploring cannula in the external sugular vein (see Fig 10B) The three records_1n Fig 40 illustrate the effect respiration had on inflow when the tip of the cyploring cannula was placed in different intri ind extrı thoracic styments of the superior vena casal syntcm In cach record the first in$piration was a normal quiet one and the sccond was with a partially occluded airway is expected when the tip of the cannula was located in the upcrior catal vein the flon inte increased proportional to the pressure gradient created by the thoracic suction (Fi, 404) When the tip was placed 3 cm cepliabid to the first rib for increased at the beginning of wspiration indicating that in tlus catrathoracie region collapse did not occur immediately Howelct is on thic jugular pressure at the cannula tıp fell to zero the flow augmentation leveled off indicating the onset of collap e Right atrial pressure declined in the usual manner (Fig 40B) Finally shen the tip of the cannula was placed in the jugular icin 11 cu cephalad to the first rib the rate of infion and jugular pre sure remained unaffected by respiration, indicating the interbosition of ·THE RESPIRATORI PLVP 87 MULLER NORMAL 2009 FEMORAL ART PRESS Ah 100- 100 ATRIAL PRESS -100 550c/SEC -200 7cc/SEC L3cc/SEC FLOW -100 JUG VEIN -O PRESS INTRATHOR -100- PRESS 0 ATRIAL F-100 PRESS --200 - 200- K23cc/SEC 09cc/SEC FLOW whichhWWhiwwwhhhhh, 100 JUG VEIN ATRIAL -100 --200 03cc/SEC FLOW TIME IN SEC FIGURE 40 Three recorda llustrating the effect of respiration on the rate of inflow into eing through an exploring cangula Rosers oir pressure 10 mm water in all records 4 = tip of cannula in superar i ens c218 B = up of cannula un jugular 1 en 3 cm cephald to tic first rib C = tip of cannula in jugular sein 11 cm cephalad to the first nb Tracing 10 each record from top to bottom ha-e lines femoral artery Thures in mm Hg venous fressures at top of cannula right atral pressures and intrathoracic pressures in mm water flow through cannula in cc /see (cnou pres ure tracing omittel in re oi! 4 ) Dedrītion in text ·88 SETOUS RH TURY 3 collap al segment of the vein betruen the cinnula tip and the thorax (Fig 40C) From these findings one may conclude that collapse does not occur at one distinct point at the entry of the thoracic cage but that the collapsing process molics i negment of the citrathoracic sein This (gment is a transition one (8) مانا مانا مانا +100- JUG VEIN 150 FEMOR ART 100 -1007 INTRA- THORAC -2004 +100 RIGHT ATRIAL -100 L-200 16cc FLOW 07cc -300- +1007 W JUG VEIN Wp-100 O ATRIAL -100 43cc --200 23cc 3406 FLOW 19cy +100-W JUG VEIN WWV wholul 200 -100 wrig 73 cc -O ATRIAL 49cc 6ccy FLOW 360CM AM by www (150FEMOR TIME IN SEC FIGURE 41 Sıx records illu trating the effect enous plethora on 16 puatory augmentation of inflot into the jugular cin Tracings as in figure 40 lo record r femoral artery tracing wag moved to bottom of record Description in tcat ·THE RESPIRATORI PLUP 59 between the noncollapsed intrathoracic and the collap cd extrathoracic region of the sein The extent of the transition zone is of cour e influenced by various condi tione an important factor being the amount of scous billing The six records shono in Fig 11 illustrate the effect of poor nous filling and of venous plethora on the collap e mechan. m In all records the tip of the exploring cannula re mained stationary in the citernal jugular vein 11 cm cephalad to the fir t nh Only the perfusion pres ure was increa edbs stages It is noted that as the vein became more plethoric sith greater purſu son pre ure the effect of inspiratory Kuction incrca ed in the persplicral portion of the vein (Fig 11 B through C) The advent of collap e can be deduced from the les eling of the jugular 1 enous pre mure curse at zero pre vure and the simultaneou plateau of the fion curte Finally when perfusion pre ure was hylets shown in Fig 1F collap was completely abolished Certain fructs are clearly demon trated by the t experiments Firet infion into a long egment of a partiall collap ed (poorly filleds sein is not affected by inspiration (Fig 11) mecond the trinition zone of collap e cxtend further ton ard the peripheral region of a vein when the vessel has a normal or greater than normal filling state Thus the extrathoracic i ein can accommodate 3 greater blood volume which is then available for empty ing into the thoracic sein durin, nopiration Thurd rising right atrial pre ure po tpones or even presents collapse In the extreme case ripre enter in Figure -11f this corresponds to the eituation eusting in conge ture heart fasure when night atrial 3 ure docs not descend below zero Summam ing Lpon in pration the extrathoracic reins do not collapse at a distanet point at the entry of the thoracic crge lihen intrathoracie pre sure dcelics a tran i tion zone is formed between the noncollapsed intrathoracic and collap cd extra thoracic region of the vein With greater spous plethora the trun ition zone extends progres Niels snto the jurypheral nas CLINICAL INFRFICES Its non pouble to reconcil confietin, reports in the literaturt on changes of peripheral 1cnous pre ure with respration (Gollutzer Veer 1932) In human when peripheral flos is normal and the heart well compensated 18 in the experixent of Lyons kennedy and Burwell (1938) in puration is ca pable of producing significant decreases in peripheral senou pre ure other womentarily by a deep agluing breath or for prolonged perrods by voluntars acceleration of the resmraton rate This chnical observation is explainable on the basis that the depleting stage may be sufficicntly prolonged to allon avg mentation of return flon by the complete re pirator act When right atrial preasure 15 lon and the on ct of in piration abrupt (Vulfers experiment) thic peripheral venous pressure decline may not la t long and the outstanding feature will be a pressure rise as the serous bed fills up di tal to 13ye regon oi maumi collape These phenomena art casıls reproducible that they can be worn in student experiments ·90 VETOUS BETLRY On the other hand if renous plethora be extreme, as in right heart fatlure, collapsc cannot occur and each in piratory effort is accompanied by a marked increquc in voluine flon toward the thoracic vcnae catae and a clear cut drop in periplıcral venous pressure In the absence of collapse in congestie failure (uch inspiration would tend to increase the inflox load on an alreads over loaded heart The beneficial effect of morphine in such cases may, in part bc ex plainable by the suppres ion of re piratory movements Burch Colin and Acuman (1942) in simultaneous plctly smograpluc studies of the finger toe and pinna noted inconstant decreases in vascular oluines in Jespon e to spontaneou deep re pirations In thic light of the above cxperiments it non becomes clear that the acceleration of venous flos caused by extrathoracic depletion may extend far into peripheral cins the incon tancies observed inay in each instance be accounted for by the supervention of collapse in some portion of the trathoracic venous true according to the peripheral senous filling status Summarizing The clinicalls observed fall in periplcral venous pre kure during quict inspira tion 14 caused by an emptsing of the veins toward the chest The rise of peripheral venous pres ure during forced inspiration is caused by a partial collapse of the veins near their entry into the che t In right heart failure venous collapse may not occur and inspiratory efforts will increase the infion load to the overloaded hicart ·VIII Effect of Artificial Respiration on Venous Return With the more extensive use of artificial re piration and controlled mechanical respiration in medical and surgical procedures interest has recently been focused on the effect of re pirators on the circulation It is generally agreed that one of the detrimental effects of controlled respiration is the mechanical inter ference of positive pressure lung inflation with venous return (for reviews see Watrous et al 1951 Whittenberger 1953) A controversy has existed for many years as to whether or not in the closed chest the interpo ition of negative pressure between the periods of intermittent positive pressure lung inflation can improve the circulation Again as in the case of spontaneous respiration, it has been argucd that ncgative airway pressure could not increase venous return because of venous collapse at the entry of the thoracic cage (Holt 1943) Somt data suggest that alternating positive negative pressure respiration may benefit the circulation (Rost 1932 Kemph et al 1992 Maloney and Handford 1954 Anschutz et 11 1955) whereas others could not substantiate this vien (Volpitto et al 1944 Votley et al 1948) All these authors used inferential evidence mo tly derived from determinations of blood pressures pulinonary ventilation or indirectly measured cardiac out put Even the venous drainage records of Rost (1932) permit various inter pretations which do not decide the issue Thus there has been a lack of unequivocal evidence to resolve the crucial question Does intermittent positive negatri e pressure respiration result in a net increase of venous return over that cxisting during intermittent positive pressure breathing ? Ile decided therefore to measure venous return directly in order to find out wicther or not intermittent po tre negative pro sure respiration ards the cir culation The experimental arrangement was essentially the same as that used for the incasurement of venous return during natural breathing In order to rule out any possible ide effects from the opening and closing of the chest a number of experiments were performed in which the chest was not previously opened In these flow was measurid with the catheter flon meter illustrated in Fig 12 The results were the same as those in other (speriments in which a thoracotomy had bcen made A Pitotmcter (Fig 11B) or a bristle flow meter (Fig 15) was in werted following the thoracotomy thc chi t was then cloud (Brecher 1993 Hubay ct al 1954. The trachca was connected either directly or va intubation to a positive native pre ure respirator FLOW I NORVOI OLEMIA The effect of intermittent po tive and intermittent po tive negative pressure breathing on enou return in the superior cna casa of a dog with normal 91 ·NORMOVOLEMIA DEPLETING STAGE COLLAPSED STAGE DE PLETING STAGE 92 COLLAPSED STAGE SECOND 116 AORTIC PRESS 104 131 97 1800 FLOW cc / min 1500 SUPERIOR VENA CAVA FLOW 1200 900 ENDO- + 2007 TRACHEAL PRESS +100- mm H20 VENOUS RETURY 7+100 600 09 wymienion 300 -100J 0 ATRIAL ATRIAL PRESS -100 mm H2O POSITIVE-ATMOSPHERIC PRESSURE RESPIRATION POSITIVE-REGATIVE PRESSURE RESPIRATION MEAN BLOOD FLOW 903 cc/min MEAN BLOOD FLOW 1200 cc / min FLOW INCREASE 30% FIGURE 42 Lugmentation of chouy return by the application of of an integritor in thic am lifier of the flowmeter Tricoge from To tive negative preure re piration in the clo ed chest of to to bottom time norte sicuri in inm Ho superior vena bormov ole mic animal Venous return is measured wit1931 sul flow in cc/inin en lotr teheal and right atrial pre ures bri tle flow meter (sce l'igure 15) in the superioi veni ( Tic 111 min Biter cardiac variations of flow are smoot) ed out partially by means ·UZEECT OF ARTIFICIAL REY IRITION OS FIOL RZTLRA 93 atrial pre blood volume is illu trated in Fig 12 This hoss A (gment of a long record at the place shere one type of re piration (alternating posin e atmo pheric pre sure) is changed over to another (alternating po atite negatne presse) Fross leítio right the trueing reveal that po stise pre yu5 lung inflation greatly reduced flow but that flou increa cd rapidly upon sudden release of the lung an flation to atmo pheric pressure This re ulted from the bachlo, of blood that rukce from the peripheral seins to the heart The flos increased (depleting stage of the extrathoracir icms) and then lescled off (collap (d stage Right ure 3.5 bxlow zero indicating the eu tence of Normal thoracic zapiration sbon the airway prt sure was atmo pilare During the next positive pre ure plac flor was again reduced lett followed the negatne pre sure phase during which flox has greatly augmented It it ohtrous that this aug mentation of fou is the re ult of the birded up blood plus the depleting of the entrathoracie senous rc cry or by the greater thoracic aspiration The Deat portni pha creduced fios again 94 shows on the right side of the record This fox reduction was sliglith greater than that ob tried during the positie plan is much alternated with atmo perie pre urc The greater flon seduction however did not cance! the ftos incrca e which occurred during the preceding Bogatne phie On the right side of Fig 12 it se noted that the forte pres ure ro e from 116/97 to 131 10+ This significant me in the arterial presaksst is er death the result of the sacrca ed renoue return The nenas delayed by about 3 to 4 heartbeats after the on«ct of the venous dou augmentation because the blood had to cur culate through the pulmonarı bed These findmg, emphassze the immediato cau 21 relationship of changes in senou3 return and sortic pressure Van flos in the superior cava calculated for tno complete positse atmos pheric pre urt cycles mas 903 ce min The corresponding wessurement duria the two po stive pegative ecles >> 13 1200 CL mm This IS A 11ct for increa e of 33 per cent In the experiment illustrated in Fig 42 onf mild poutre pressure lung in ſtation was cmplosed Flon was measured in numerous e\periments over long penode of intermittent po itile and positne negatne preasure breathing liath the latter type of respiration fox was alu345 zugucated It was generally found that the net son dereaat br came relatniy greator during poutnu negativc hreathing si the lungs sete dilated math hgtır pre urta during the po itse phases Sunnlar for augmentation du ck monstrated in the superior sina cit in Fig 12 were al seen when m. ured tires in the softrior cana separately or in both casal seine smultancously Summar ing The application of intermittent positize negatite pre sure re pnration au. Tulents venous return significath ayer that existing during internittent po i the atino pheric pressure respiration The set increase of venous return cauad by the negative phase is brought about in thorkie aspiration acting umlarly to the mechanı m operatie in spontaneous respiration ·16 HYPOVOLEMIA ECOND AORTIC PRESS 398 SUPERIOR VENA CAVA FLOW FLOW co/min r+200 ENDOTRACHEAL PRESS mm Hg VENOUS NETURN 900 htBo ATRIAL PRESS yoo -100 1001 -160 POSITIVE ATMOSPHERIC PRESSURE RESPIRATION POSITIVE-NEGATIVE PRESSURE RESPIRATION MEAN BLOOD FLOW 133 cc/min MEAN BLOOD FLOW 266 cc/ala FLOW INCREASE 100% FIGURF 43 Augmentation of renous return by the application ineren c of flow in hypovolemi as compared to normox olumn of 10 ite negative pressure re puration in the cloud chet of hown in lue 1" (Things as in Iure 42 ) a hypovolemic animal ilustrating the relatively greuter net ·EFFECT OF ARTIFICIAL RESPIRATION OV IEVOLS RETUR Da Frow I HIPOKOLENIA It has been often observed that an increase of po itne pressure in the airu ay of patients in slock or in poor circulatory condition is dangerous (Beecher et al 1943) Experimental support for thus ob ination was furnished by Carr and Excx (1946) and Valont) and landford (1994) *1?10 demonstrated that positive prcesure respiration is specially detrimental hea hypov olema is present It was therefore of interest to see whether the use of a negatnc phase between postis e pressure fun, inflations would tend to alleurate these adverse cffects This was studied by creating hs por olmc status in co cd chest dogs by bleeding them until their mean arterial blood pressure was reduced to about 0 mm Hg Figure 43 depicts a segment of a record 1}}ustrating the deleterious effect of positic atmo pheric pressure breathing and the beneficial effect of positive negative pris ure respiration on venous return during hs por olema For easier comparison the record is taken from the same experiment which is illustrated in Fil 42 It is scen (left) that enous return was very mall during positive atmospheric pressure rc piration but was great! augmcated (right) by negatne pressure llthough mein blood flow during positive atmo pherso respatron was only 133 cc/min mean flot during poitr e negative breathing increaned to 266 cc /121n when each was measured Oier two complete reapura tor cycles this is a 100 per cent net increase of flon It should be recalled that in normos olemia the addition of negrtne pressure in the closed cost of the same animal resulted in a net flow increase of 33 per cent The absolute fos increase by the use of the negatire pressure phase in hy povolemia (133 ce ) was not so great as in normosolemia (297 cc) since the content of the peripheral reservoirs es greatly reduced Hos cxer the Bon augmentation was relatneh greater in h por olema mce the instial volume flon rate was very low Thrue facts derned from the fou curses in Fig 43 should be emphasized (1) Pontse lung pflation resulted in almo t complete cessation of flos (2) Atmospheric presvuit did not create a favorable enough pre sure gradient be tween the peripheryti semns and the right atriuši to deplete adequately the backed up blood into the thoracic veins (3) Decrease of the pressure gradient from the peripheral vems to the heart cmptied the small peripheral crous re em oirs more effectuely As already demonstrated in the rase of normov olema arterial preure niso roce in s porolema 1s 1 result of the increase 3 scnous return (from 43/35 to 58/39) Summansing Vse of intermittent positie negatie presunc respiration in hy por olma augments venous return relatively more than docs the same type of respiration 3) Ormov oleman VIVOLS RETURY IN THE OLEN CHEST From the caperiment presented in Figs 42 and 43 it is apprrent that in crcased thoracic aspiration is the mechanism rejonyble for the augmentation ·96 OPEN CHEST I SECOND — ARTERIAL PRESS (130 100 SUPERIOR VENA CAVA FLOW FLOW co/min r1200 r+200 ENDOTRACHEAL PRESS mm H2O VENOUS RETURY 909 600 -100 ATRIAL PAESS mm Ho POSITIVE ATMOSPHERIC PRESSURE RESPIRATION POSITIVE - NEQATIVE PRESSURE RESPIRATION MEAN BLOOD FLOW 800 cc/mia MEAN BLOOD FLOW BIO co / nta INCREASE NEGLIGIBLE ICUAC 41 Insiguilieit inte of venous return upon applı sunt lung intitons in the open chet (Trienna Insure 4?) sition of nie en loti che il presure between jo itse pris ·EFFECT OF ARTIFICIAL RESPIRATION OY HEVOLS PETLRS 97 of venous return during positne negatne breathing If this is true it should lye expected that after thoracic suction is abolished by opcaing the chest enous return could not be improved by the use of positne negative pressure respiri tron This is demonstrated by a record in Fig 44 The segment corresponds agun to tho e shown in 1, 42 and 43 The very end of a positive pre ure lung in Pation and the sudden relea e of endotracheal pressure to atmospheric value ss sein at the extreme leit of the record superior cna ciral fou wluch was seduced during the lung inflation increased mmcdiatch upon release of the postate pres ure in the airt an The next lung intution «ecn in the muddle of the record showed the same reduction of fon This inflation was folloued by the appeation of negatre pressure to the unas (right ide of record) It did not result in a substantial inerti e of Hon over that observed during atmos plerie endotracht 13 ye sure During to complete pitne atmo pheric respira tort cycles superior casal fos amounted to 800 cc mir wherers during two poitre negative cycles it 11 18 810 cc min Other eaperiments in which enous return was nicayured simultaneously with cardiac output also shoned that ordinc output did not improve by intermittent po tive negatne pressure rcs guration in the open client (Hubay and Brock 1996 Sonori ing In the open cheat the net fos incrcase by the application of postre negatne Muie respiration is negligible EVOL RETIRS AND CARDIAC OUTPUT Drain ANTIMICIAL RESPIRATION Baxter and Pear < (1951) obersed a significant pulmonary arterial for augnentation during the negative phase of intermittent po itne negative pres sure re puration in the closed chest of the rat They felt that this might be due to an increase of venous return Therefore studies were made to sce zf such a causal relationslip actually ext Brecher und lubay 1906) The effects of interisittent posituse atio pheric and interuuttent positive negatire pressure respiration on renous return and cardiac output in a closeul Chico normos olemaic dar are illustrated in Fig 43 is m te records shown in Figs 42 and 44 a segment was chosen in ninth one type of respiration was changed to another A representative of scnous return uptror casal flow 32 rccord with lyristle flow meter of the ts pe depicted in Fig 15 Smultaneousy total night heart output was recorded by measuring flow directly in the trunk of the pulmonary arters sath the modified bristle flox meter illustrated in Figs 16 and 17 I enous flon (second curse froni bottom) followed the same pattern described bcfore It was reduced during po itne pressure lung inflation and incra ed particularly wlien suction 11 13 applied to the trackca Cardiac output {third curve from bottom) sas also reduced during the lung inflations but not to the same extent as senous return it was also increased during the negative plase It is noted that the change in cardiac output always took place one heart beat after the changes in Tenous return This lag has particularly strzhing when enous return increased upon the application of negatne endotracheal pres ·98 LEVOUS RETURN 5 SECONDS 1507 AORT PRESS 100 MAA W 0 INTRA- THOR PRESS -200 -600 PULM ART PRESS 300 ENDO- +100 TRACHT PRESS r1800 O 4507 SUP CAVA FLOW 300 CC/MIN 150- -100 PULM ART 1200 FLOW CC/MIN 600 +50 SUP HCAVA PRESS -50 FIGURE 45 Relation of venous return to cardiac output during intermittent po atiye almos pheric and positive negative pressure respiration in the closed chest Tracings from top to bottom time and base e aostic pressure 10 min Hg intrathoracie and endotrachenl pres. sules in mm water pulmonary arterial and superior vena caval flows 1a cc/min superior veni casal pre sure in mm water De cription in teat (Unpublished accord of Hubay and Brocher ) sure and dccrcased when prcs ure in the trachea returned to atmospheric level Endotracheal pressure (fourth tracing from bottom) was transmitted into the thoracic cauty as indicited by the changes in intrathoraric pressure (fifth tracing from bottom) The pressures in the superior cava pulmonary artery and aorta folloned the capeeted trends ifter a delay of scieral heart beats aortic pressures rouc from 145/116 to 155/122 as a iesult of the augmented chous neturn and night heart output (Fig 15 right side uppermost curve) From the time sequence of thic hemodynamic cients displayed in the prussure and flou tracings one can conclude that the increase of right licart output is the direct icsult of the augmentation of venous return shich itself is caused by increased thoracie auction The measurement of mean fion during 3 complete re piratory cycles revealed that superior casal flow was increased from 510 to 630 cc/min and cardiac output froin 1430 to 1630 cc/min by the use of thoracic uction bctn cen lung inflation ·EFFECT OF ARTIFICIAL RESPIRATION OV EVOUS RETURN 99 Summaning Intermittent positive negative pressure respiration augments right heart out put significantly over that prevailing during intermittent positive pressure breathing The changes in cardiac output are directly caused by the alterations in venous return during these tao types of respiration Flow DURING LUNG IVFLATION IN THE OPCY CHEST It has been often observed that in the open chest venous return decreases during positive pressure lung inflation (sce Fig 44) (Brecher and Mixter 1903 Vixter 1903, Brccher 1954 Hubay et al 1931) The genesis of this decrease in flow is not clear It could be caused by a primary hindrance to inflow into the right heart such as Humphreye and his associates (1939) have sugge ted or be secondary to an increase in resistance to flow in the pulmonary bed as suggested by Anhenny ct al (1931) Experiments were therefore designed to determine how much of the flow reduction is actually caused by an impairment of right heart filling and how much by an inercase in pulmonary re istance (Hubay ct al 1935) Figure 16 shows a diagram of the experimental arrangement Flow was meas urcu with two bristle flow meters in the right and left branch of the pulmonary artery Changes in pulmonary resistance through lung inflation could be elimi nated by trmporarily shunting blood from the right pulmonary artery into the left atrium while clamping the left pulmonary artery simultaneously The aim was to discover if outflow from the right heart (approximating venous return) would change during lung inflation cien if resistance to output remuined con tant as it does in the tubing of the shunt The record shown in Fig 47 illustrates the effect of positre pressure lung in flation when the total pulmonary blood flow passed through the right lung The filos tracing appcars as a heavy black undulating line (electrical signal inte brated in amplifier) Segment A is the control flow with atmospheric pressure in the airway Blood flow was 1 403 cc/min With lung inflation flow was reduced to 1 237 cc/min as shown in segment B a flow reduction of 11 9 per cent Figure 48 shows two corresponding segments of the same record tahen ten seconds later after flow was diverted by merely opening the shunt to the left atrium and clamping the tubing leading to the right pulmonary vascular bed Section A is again a control fou measurement during atmo pheric pressure in the air way Flow amounted to 1 652 cc /min it was reduced during lung inflation in segment B to 1 610 cc/min The 27 per cent reduction shown in this record is so close to the limit of pre cision of the method as to carry little sught However in all of the records of this type of experiment a reduction was observed consistently during each lung inflation On this basis the recorded reduction is considered to be real One may deduce from these findings that the 11 9 per cent flow reduction during lung inflation in Fig 47B was mainly caused by an increase of resistance in the pulmonary vascular bed because flou Tas less reduced (27 per cent) when the resistance remained constant (shunt flon section B Fig 48B) Hence the major factor reducing venous return during lung inflation in the open chest is the increase of resistance in the vascular bed Other factors which obtlously ·100 VE VOUS RETURN RIGHT LUNG TRACHEA RESPIRATOR RIGHT PULMONARY ARTERY SHUNT (BRISTLE MANOMETERS LEFT ATRIUM RIGHT ATRIUM FLOW METERS RIGHT VENTRICLE OPTICAL LEFT PULMONARY ARTERY LEFT LUNG AORTA FIGURE 46 Diagram of experimental arrangement for shunting pulmonary blood flow (open chest dog) For technical simplicity the shunt leads from the right pulmonrry artery to the left atrium Throughout the experiment flow through both lungs is imultaneously recorded with two flow meters For te ting the effect of pulmonary bed resistance venous return total right beart output is diverted to the right pulmonary artery by temporarily occluding the left pulmonary artery The right lung can then either be perfused by clamping the shunt or by pas ed by clamping the right pulmonary artery at A mu t reside outside the pulmonary circuit play a minor role Nevertheless their cxistenec should not be neglceted They can be characterized as a mechanical compri ion or tamponade of the heart ind great vessels by the expanding lungs much occurs even in the open chet Summar ing Iwo etiological factors account for the reduction of venous return during positive pre sure lung inflation in the open chest Quantitatively the most im portant factor is an increase in pulmonary bed resistance which secondarily diuinishes venous return A less important factor is the tamponade of the heart and great vessels which primarily reduces right heart filling CLINICAL I VPLICATIONS At first glance these basic expurimental findings inay not scem to be of great clinical importance Vide clinical experience has shon n that in the closed chest ·EFFECT OF ARTIFICIAL RESPIRATIO IV VELGUS RETURV 101 1800 SECOND FLOW CC PER MIN M m 900 RIGHT -600 INTRA- 300 VENTR 0 AS 1200 2007 LEFT 1004 Wer bara ATAL 100 600- RIGHT ATA 245 50 0 ENDOTRACH FIGI RS 4. Lfest of po se pressure lung inflation on total pulmonar blood flow 1) rowg! 1) e rigit lung lien the left pulmonar arters is occluded (apen che t) Segmest flow and pres use tracings during aftio phcrie airway pressure (endotrachea) ) Segmat B Aime tracings during luog jaftation with cadotracheal pressure of 245 mm vater Tracings from top to bottom timp right intrareatricular pres ure in mm fater mead fotal puliponars blood flow in < /ein left and riglet atral pressures i min water codotracheal pre ure in mm water 15 = atrial systole Time sofer al between end of segtucat A and beginning of egtnent B. 09 sec the u e of intermittent positre pre ure re piration is fe 11 norinos ocne patients and induuduais in good circulatory condition The dctrumental cffcct of po stase pressure in the 31111&) is easily overcome by Ane in peripheral Tenous pressure ancreá cd autonotte activity and mobilization of blood teser voirs leading to a more {az arable pressure gradient betseen the periplierał seins and the right atriuin sits 391 adequate blood flon into the central seis A sight reduction of cardiac output is uostoportant during many operative pro cedures or even destrable during ome of them However under conditions of blood lo s hypotension or shock resery ours are not available to allow this compensatory rise un pressure gradient favorig inflon and the poor vchous return 14 d32332<hed further by intermittent 101 tre pressure re piration Tlie animal cypictinents furni k direct er dence that in such cases the use of interwttent positue negative pre vure breathing can improve venous return and cardiar output The con iderable net increa e of Venous return makes a greater turnover of the as aslable blood posible With the chest open cnous return is always impeded by po itne pre sure lung inflation The amunal experimcíls have clearly demonstrated that in the ·102 VESOLS RETURY 1800- I SECOND FLOW CC PER MIN on you 8900 RIGHT +600 INTRA- 1300 VENTR. AS 1200 200- LEFT 100- ATR. Personal Morgan -100 0 600 RIGHT hr ATR with 550 250 ENDOTRACH FIGURE 48 Efect of powithe pressure lung inflation on total pulmonary artery flow which by plaves the lunge (open chest) The left pulmonary artery is occluded and the total blood 18 Hunted through a tube from the night pulmonary artery to the left atrium begment 4 flow and presure tracings with atto pheric pres ure in arway (endotracheal O) Segment B same tracings with endotracheal presure of 200 mm water Sequence of tracings as in ligure 46 Asatral systole Time interval between cad of segment 1 and beginning of segment Bts 0.8 vec open chest the interposition of a suction phase between lung inflatione docs not benefit crous return or cardiac output becau e the mechanism of thoracic aspiration is absent Therefore, from thus hemodynamic point of vicu po i tive negative respiration offers no advantage os er positive atmospheric res piration in patients undergoing thoracic surger This is not to deny that posi tive negatne pres ure ventilation during open thoracotomy may have a beneficial effect in other respects for example in reducing the CO tension in the arterial blood as demonstrated by calon ct al (1900) Since the decrea e of right heart output during lung infation in the open cliest could be attributed to both an increase of pulmonary bed re istance and 3 tamponade of the heart and great scssels caution should be employed in in flating the lung The clinical practice of u ing prolonged positive pressure to acrate atelectatic lungs should be avoided as hould also excessile inflation of the lungs which may interfere with the hearts filling Admittedly in patients with an adaquate circulatory reserie compensation for such derangement is commonly ob erred but in patients who have lo t blood or who are otherwise in a poor circulatory condition the effect may be very detrimental ·EFFECT OF ARTIFICIAL RESPIRATIOV OV VENOUS RETURN 103 Summarı ing In the closed chest the use of intermittent po itive negative pressure respira tion may benefit patients who are in poor circulatory condition because it facılı tatcs their venous return However this type of respiration is not beneficial for incres ing venous return in patients during open thoracotomy Excessive lung inflation in the open chest interferes with venous return by an increase of pul monary bed resistance as well as by a tamponade of the heart and great vessels ·IX Effect of the Heart's Action on Venous Return In order to study the forces by which the heart itself may contribute to the return flow of blood it is necessary to obtain accurate information about the rapid variations of venous return within the cardiac cycle (scc page 27) The 5731 bristle flow meter was specifically des cloped for this purpose (sce big 13) In these experiments meticulous care was taken to preserve thic anatomical relations of the heart and its neighboring structures The pericardium was not opened and whenet er the chicst was closed the normal intrathoracic pro sure relations were re established These points are important for an evaluation of the forces wluch are normally responsible for cardiogenic flos changes CEVTRAL TEVOUS FLON PATTERN When a bristle flow ineter was inscrted into the superior vena cava at the entrance of the right atrium numerous types of fiok curves ucre obtained A representative curic is shonn in Hg 49 illustrating flow changes during the cirdiac cycle in the open che t The time correlation is given by the multane ously recorded right intraventricular and superior ca al pressure curie Right atral inflow became greatly accelerated during ventricular contraction Tig 49 2 to 4) and again slightly accelerated during ventricular diastole The great est flow reduction occurred during atrial sy stole Similar flox patterns were recorded in the inferior vena cava The amount of blood entering the right atrium from the superior veni car? can be determined by measuring the area under the flon curve It found that venous return was greater during sentricular sy stole when the tricu pid vites were closed and no blood could enter the vcntricle (230 cc volum in flow from 1 to 4 in Fig 49) than during ventricular diastole when the tricuspid alies were open and atrium and ventricle formed a common cavity (21 cc from 1 to 9 in Fig 49) Summancing Typical vena caval flow curses show tho main summit one during 1 citricu lar sy stole and the other during diastole Venous inflow into the right atriuin is large during the time when the tricuspid salves are closed TIIE ACTIC VENTRICULAR SISTOLE The fact that the rate of voluine flor in the central veins is greatly accclcrated during ventricular sy stole s hen the blood is blocked from entering the Icntricle indicates the eustence of a strong frontal force which causes the acceleration The explanation is as follons The responsible force is the contraction of the cntricle itself which drans blood tonard the heart The descont of tlic atrio ventricular junction during ventricular sy tole cnlırges the grcat venous reser 101 ·EFFECT OF THE HEARTS ACTIOV OV YEVOUS RETURN 105 | SECOND 123456789 IT -400 NU -200 0 1500 CC/MIN 1200- FLOW 900- 600- 30 50 qill 2 3 5678 4 FIGURE 49 Venous return during different parts of the cardiac cycle (open chest) Tracings from top to bottom time right intraventricular pressure in mm water superior vena casa flow in cc/mia superior cava pressure in mm water Numbers 1 to 9 denote the phases of the cardiac cycle S = s stole D = diastole voirs namely the atria and venac carae Thus the piston like downward move ment of the atrioventricular junction attracts blood from the central cins into the atriumn ( ce lig 1) This vice 1 upported by the following additional cuidence from unpublished records of our laboratory (11 In 2 2 1 or 3 1 block caval flow is stopped or bricfly rever ed during cach atrial sy tole II lien the atrial systole is not fol loned by 1 ventricular contraction caral blood is not accelerated after the atrial muscle Ins relaxed (see also Nilsson and Kramer 1954) (2) In atrial fibrillation where the rapid atrial muscular contractions barcly affect flow in central vans blood is distinctly accelerated during ventricular sy stole (3) The acceleration of venous flow during sentricular sy stole can be decreased by open ·106 VENOUS RETURN ing the pericardium or by removing the support of the heart in other ways In such cases the apex of the heart is often seen to move upward or sideways and the descent of the atrioventricular junction becomes less pronounced The quantitative measurements of blood flow have thus furnished the here tofore missing direct evidence in support of the concept that the contraction of the myocardium itself draws blood toward the heart It establishes the existence of a substantial vis a fronte of cardiac origin The function of ventricular contraction is, therefore, twofold It consists not only of the cjection of blood from the ventricle but al o of the 'injection of blood from the seins into the right atrium In other words the heart does not merely act as a pressure pump as William Harvey believed (1628) but it actually functions as a reciprocating pump (pressure suction pump) This is illustrated by & rccord shown in Fig 50 Superior caval flow was recorded imultancously with total pulmonary artery flow It is noted that right atrial inflon was greatly augmented each time the right ventricle ejected its content The two tracings fit into cach other like finger and glove making it easy to concere the heart as a pressure suction puinp One may objcct to the use of the term suction in this conection Suction implies the des clopment of negative pre sure A retracting piston connected to SECOND 125 AORTIC PRESSURE 100 75 -4800 -3600 CC/MIN FLOW IN MAIN - 2400 PULMONARY ARTERY F1200 1800 CC /MIN FLOW IN 1200 SUPERIOR 600 VENA CAVA O 600 SUPERIOR 50 VENA CAVA PRESSURE FIGURE O Iction of the heart as a pressure-suction pump visualized by the simultancous recording of inflow and outflos (open chest) Note the acceleration of venous return during tentricular ejection Right heart output recorded pbasically with bristle flow meter slowd LA figures 16 and 17 Superior vena caval flow recorded phasically with bristle flow meter hown in figure 1. Tracings from top to bottom time aortic pressure in mm Hg pulmonar ar terial and superior cas al flows in cc/min superior cas al pres ure in mm water (Unpublished record of Hubay and Bret her) ] اگر با مدل پالمرور ·EFFECT OF THE EARTS ACTIOYO SE VOUS RETURN 107 1 nigd walled tube system creates a ncgative transinuralpre sure The 82mo piston (A V junction) connected to a collapsible tube system (atrium) car not create a negatne transluural pressure because the collapsible walls (atrial Walls) are compressed by the extramural pressure In other cuso the luid 18 pulled toward the piston by the creation of a lou pressure near the rutractın, piston In either case the force (ventricular contraction) winci mos es the piston creates suction regardless of the transmural pressure wirch becomes negative only in a rigid walled system but cannot descend below Zero (atina pheric les cl) in a collapsible systein This situation obtaine in the atria and vans which are collapsible structures For the reason one cannot record negative transmural pres ures in the seria during ventricular systolc Atral pressures can only discend to a very low value but not to less than 2cro in the open cheat Subatio pliersc atrial pressures occasionally recorded in open chest animals during ventricular systole are under vi pieion of being duc to sccording ustifacts At most thcy are only a few inn of water below zero and of very brici dura tron Summar ing Direct and quantstatsse cuidance indicates that thic scntricular myocardul contraction provides a 128 a fronte ulich draws blood actively toward th. heart during ventricular systole Hence the heart does not act as a pressure pump only, but as a pressure suction pump during ventricular contraction VESOLS RETUR Duus VEYTBICULAB DIASTOLE It will be recalled that there 14 a rclatiucis email acceleration of venouy flow at the begioning of ventricular diastole face FI 49) It liay generally been ob serucd that with lower heart ratcs venous return bacones incrcasingly mors, prominent during ventncular distol (llolzlohner und Sclsoncratcdt 1911, Brecher and Praglip 19.3 Bruches 19,1 on and hreiner, 1938) TIC effect of different heart rates on thic tyttolic and diastolic affox into the atrium was ther<fore studsid uriks stru tly controllut cxpxruinental conditions (Brecher 1991) In opin che t dogs with Baturally rlow kwart tau tin nghit atrium Katy stimulated with clectncul blochs in order to siroduce fastur heart rules without altering day other factors in the cxpxTHunt llure SI illustrates the effect of differest focart ratcs on venous return Wonent A defecte conuruture heart beats the fir t one with a long dia tol and the recond one with a short duurtolu. Segincnt & roseals thic fos psttest bon the atriuri 48 staraulstad 3 tsines per cond It 3 nutci that the durstion of Az utolc skanunlstrely little sith the acceleration of the heart and thut vchoux return cung cach indul As Cola remained approxmstely the slot On the other hand lic dis tohc return flow was las e with bradycards 1993 vity all with taylandia Pvtal superior cal al rolusso fost får "cond toss asard udst the varit at all blast rauc slow (83) best rate 33 per cont of the box interul thr striuin during sy Wola and 27 per cent dunn, <li s lok At luskyldu (177) the corretfrndung fo ucre 81 pxr unt durinn, +5rtul nr 19 * Iteht durinidia tole Thus cxpuriinnt denon laten that the lart ft **{id rell regulatory ·108 EXOUS RETURN 15 sec A DI MONITOR ® 200 AORTA Foo FLOW 1200 CC/ MIN 900- 600- 300 SIDSID SD 1007 50 PAS SUP CAVA PRES FIGURE 51 Effect of heart rate on inflow into the right atrium Venous return is plaically recorded th a bristle flow meter in the superior vena casa (open chest) Description in text Tracings from top to bottom time sortic pressure in mm Hg uperior cna cia Row in cc/min superior da casa pressure in mm water Note the brief reveral of flow during the peak of atrial systole (indicated as PAS in the superior i ens cas al pressure curse) mechanism which heeps venous retuin constant within luts It does so by sub stituting during tachycardia the rapidly repeated active systolic attraction of blood for the diastolic inflow into the atrium hich predominates at normal and slow heart rates This mechanism must be looked upon as an innate afety device of the heart by which it assurcs its own atrial filling with sudden cardiac acceleration such as may occur during stress 01 anxiety knowledge of this mechanism mahçs it understandable why cardiac output can be maintained fairly well at fast heart rates Under comparable conditions atrial inflon is usually larger in the closed than in the open chest during i cntricular diastole This is illustrated in Fig 52 Flow as mca ured in the superior cual rein after chest closure Inflon during sy stole (S) was less than during diastole (D) In the middle of the record the endotracheal pressure was lowered and flow during the next tro heart cycles increased due to thoracic aspiration The fact that in the closed che t strial ·EFFECT OF TIJE IIEARTS ACTIO OS VEXOL RETURN 109 I SECOND 92112 1800- CC/ MIN AORT PR 1500 SUP CAVA FLOW- 12001 900- ENDOTRACH PRESS 600 O 300 - 100 130 SUP CAVA PR -100% -200 FICE RE 52 Effect of increa ed thoracic aspiration on cnous return during ventricular la tole (closed ce t) Endotracheal pressure in a closed s tetn is lowered from atmo pheric (zero) to -1,0 min water Tracings from top to bottom time aortir pressure in mm Hg uperior vena cas al flow in cc/min endotracheal and superior vena cival pres,ures 13 mm water S=systole D = la tole infion is often larger during diastole than during systole vuggests that negatre intrathoracic pres ure enters as an additional factor promoting venous return It acts apparently by a direct suction on the outside of the ventricular and atrial walls thereby cxpanding the heart » cavities passively and in turn permitting greater inflow from the venae cavac Furthermore the systolic attraction of venous blood by the de cent of the atrio ventricular junction may be less pro nounced in the closed than in the open cheat This is supported by the ob en a tion of Ru hmer (1953b) that the atrios cntricular junction docs not more so exten 11ely in the closed us in the open chest The question of whether or not the ventricle suchs blood from the atrium dur ing diastole has not been re olved by the c experiments It is generally concluded from the observations of von den Velden (1906) Straub (1912) liggers (1928) Cotton (1934) und Lazst and Vuller (190) that the absence of negative pres sure in the ventricular cavity is sufficient cvidence for the nonexistence of ven tricular dia tolie uction ·110 TESOUS RETURV Honcier, a brief thcorctical consideration reveals that the lack of negatie intraventricular pressure, dctcctable with present techniques, does not nece sır ily prove the absence of a diastolic suching force It has been pointed out on page 107 that negati e pressure cannot disclop in the atria because their walls are plu abic (= collapsible) It can be stated likewise that a detectable negative trans mural pressure cannot deselop in the sentricular cavity ince the more rigidly alled ventriclc forms a common cavity with the collapsible structures of the atrium ind veins during diastoli and resistance to flow from the atrium to the sentricle is negligible Lien if the sentricle docs sack in blood during diastole it may not produce a detectable negative transmural pressure in the sentricle because the pliable walls adjoining atrium permit a form change of the atrium when it cmpties its content into the sentricle Summarizing The heart heps its i nous return relatively const int by simfting the propor tron of its atrial inflon from the predominant infon during the long sentricular diastası of bradycardia to a large active infos with tachycarddue to the rapidly repeated stolic attraction of venous blood Owing to thoracic suction on the cardiac walls diastolic inflon is often larger than systolic inflow in the closed chest Tlie commonly accepted evidence for the noncxistence of ventricu lar diastolic suction (16 absence of negative intraventricular transmural pris sure) is not neces arily conclusive Negatic transmural diastolic pressures and diastolic suction can occur in the intact nummalian ventricle wlien the residual volume is small PILASIC INLON W STROKL VOLUME Dukis NATURAL BREATHING Since cardınc output depends on venous return onc as faced with the question of how cardiac output is related to the cardiogenic and re pirogenic flow changes in the central veins under normal physiological conditions This is of particular interest since it has been disputed whether in the closed chest, cardiac output could increase with spontaneous inspiration in view of the fact that the pulmo nary arterial bed re istance is known to 1150 with inspiration (Edy ards 1951 Baxter and Pear e 1951) In order to elucidate the inner in uſuel the dynamic changes in ycnous rc turn and curdic output are correlated during natural breathing phasic flow in the uperior vena cava and the main pulmonary artery were simultaneously recorded with two bristle flow macters (Brucher and Hubay 1935) While the minuscript was processed negatuse jatrientra ular tran mual pre uc ranging in 2 crage from 5 to -96 mm water were demonstrate an open che t dog (Brocher 1956) Su h negatise pressures and dirstolic suction could be demonstrated only when the collapsible structures (left atrium and pulmonary cins) were closed off from the ventricle This was done for several heart beats by occluding the mitral orifice The negatne intra ventricular presure and suction is apparentis caused by an elastic recoil of the ventnuiar walls Thcsc experiments prove the existence of negatne tro mural scatriculi prem ures and of diastolic intrayentricttlar suction in the intat tammalaa herrt hen the ve 22) olume is small Honeycr do conclu ion can be down as to the quantitati o significace of diastolic suction for filling of a ventricle which contains a normal or large residus.olume ·EFFECT OF THE IL ART ACTIOV O TELOLELTIR I SECOND ELL AORT 1507 PRESS 100- PULM r 600 PRESS +507 SUP 0 CAVA -50- PRESS -20 -204 r18000 PULM 9000 FLOW LO 360 358 406 420 32 2 42007 SUP CAVA FLOW 2100 SD ایربراہیں 135 198 241 123 FIGCRE 53 Lffect of ontaneous rc piration of venou return and ctrlac output (closed chest) Tracings from top to bottom time and base line aortir pres ure in mm llg pulmo nan artery superior ina casal and ratrathoracic pressures in mm water pulmonary arterial and superior vena cual fons in cc/min 4 = beginning of in piration S = acceleration of superior cna casal flow luring ventri ular sy stole D = ecceleration of superior vena caval How during ventricular lastole Strohe olume (in ce ) under pulmonan arterial flow cure Flow (in Lc ) thiough superior veni cava during cat car liar cicle at Iottom of record Elec trical fic quenes ressons of both flow meters reduced from 100 to 40 rycles, scc Superior na al preure cuse duped Figure 53 is a segment of a record which illustrates the flos changes during fire heart beats modificd by the action of one te piratory cycle Flon in the superior veni cars (lowest tracing) is seen to increase during cach ventricular 5) stolc (S) and again during eachi sentricular diastole (D) The amount of Woodh passing through the superior cava during cach heart is cle (cc/cycle) Wis calculated from measurements of the arca under the flox curve and entered in the record of FG v3 under the tracing lath the onset of inspiration (A) nous font increased as early as the beginning of the sccond hcart bcat It cached its mixinuin during the third beat when inspiration became deepet During cypration venous flow becime minimal and increased again during the re piratory pause ·112 YENOUS RETURN The changes in the strohe volume of the five licart beats are visible in the next to last tracing of lig 53 Right licart output did not increase during thic nccond henrt beat di pite the fact that i cnous return during thic samc heart cycle 114 already greatly augmented The output became largest during the fourth beat though venous return had become minimal and cxpiration had already started The smallest volume is ejected by the last bcat ulicn venous return 178 ngun on the increase This record demonstrates that pulmonary artery flos incrcised significantly during spontaneous in piration in spite of a mall (but not signific int) increase in pulmonary artery bed resistance Furthermore the increase or duercasc in right heart output always camc one hcart cyclu aiter the increase or decrease in venous return since the blood had to pass through the heart Tlus sequence of cients indicates that the augmentation of pulinovary artery low wath natural breathing was directly caused by the increased cnous return and was not due to a reflex or an intrinsic inechanism of the right ventriclc The calculation of the stroke volume and caval flows per lu art cycle lows that during inspiration right atrial inflos 178 relatively larger than outflow from the right ventuele * Thus, the incrcase in venous return must result in a dilation of the right heart during in piration From this sc must conclude that the right heart iets as a moderator for the pulmonary flow by tanporarily storing part of the large influx of venous blood during inspiration and ejecting the stored part during (xpiration and the expiratory pau e Summarı ing Right heart stiohe volume increases during pont incous inspiration becau e venous icturn is augmented by the in piration The right heart accommodates part of the large respirogenic influx of venous blood tempor arily and releast » it into the pulmonary circulation during the respiratori piu NEWR Co CEPTS OF THE HEARTS ICTION ON EVOL> RETLE" The pre ently available cadenci mahes it necessary to adjust ome of our thinking about the role of the leart in the return flow of blood Thic fact that ventricular contraction actively drans blood into the right atrium mahes the heart it elf a factor of primary importance in the regulation of venous return Durin, ventricular sy stole the atrium not only fills passively with blood pushed by the left scntricle (vis a tergo) but due to the descent of the atuou entriculır Junction it also ladles blood from the ci tern of the central seins in accordance urth its availability for the subsequent ejection ( ce Fug 51) Thus a moru sovereign role must be as good to the heart thin generally belici ed The filling of the atrium during ventricular sy tole depends not only on the quantity and pris ure of blood on the cnous reaert oir hich may be sailable for pa sic inflow but also on the 11 or with shich ventricular sy tole moics the atrioventricular junction Thus i vigorous contraction (commonly 25 0 ciated with a large stiohe output) in ures additional inflow into the atrium The sume quantitative relation between uperior casal flow and right heart ejection was al o established for the inferior vena cala in otlier experiments (Hubzy and Brecher uppublished data) ·EFFECT OF THI HEART ICTIOY OS TEOL RETUTIN 113 of any available blood and therefore ſicilstates the neat large ventricular Czec trou sithout causing in catrcme diminution in intricular rssdual content The imate need of an ucrta l in cardiac output is therefore jutomatically å und by the mult sacous incru e of atriul silou both medited by the same force the ventricular contraction The central vins are inot uitable for thire croir function becau e their content can change rapidly through a partial collape of their sails accompınied by s very email ch moc of pre ure They form a collapse ckamber which is the functional counterpart of the aortic compression chamber {Brecher et al 1953) On the arterial de it to the compri ion chamber inindhi il ba ed on the elastic di tensibility of the walls ulch i uri tik tr’ınsformation of the dis cortinuous cardtucijactrons into teady fou for the tis ucs On the vcnous side it as the collapse chamber based on the subsists of the malls which a ures the transformation of the steady flou from the £180es into the pulsatile fou at the atrial entrance which is nec du for the di continuous cardaar filling compte extent of cardiogenic and s progenic Non els anges in abdominal and thoracie inferior vena cair in F. 33) The filling of the collap e chumber isded by the urial sy tole From a hemodynamic standpoint the function of trial contrartion as twofold (1) It adds a little blood to cntricular fiffin ithanell establs fed lart: 121 It cnlarges the central venous re croir bs briefly topping atrial flox Hence an adequate mount of blood is readih utulable for the raud empting of the ci tern by the net sentricular contraction The mall amount of bichlou which is often recorded during tral tole at the cual atrial junction does not atend far into the periphers (Brecher 1971) It is readily taken up by a wzdening of the collap o chamber and together with the continued infion from the periphery create the pool frona 1 iuch the next entricular filling dernes its supply It iDay be a sumed that the itution ob ered for right atrial inflou pre ails al o for infilos to the left atrium ( cca o pige 23+ Thus e entially true becau e the fion pattern in the pulmonarı veins are imilar to tho c of the casal sens Honeser in recent (unpublished) eperuents in such for was recorded with ont briatic flow meter in pulmonart ein ind with another in a enalvern uc found that atras infos durin, ventricular dia-tok nas relats els larger into the left than into the right atrium One could speculate that either the greater tis a tergo through the lon resistance pulmonary ascult bid or 3 greater facilitation of sentricular dastolic inflow igrerter suction of the tinch Talled left uentricle) ny account for this difference Although for reasons of clarits the rematon and cardiae factors are con dered here cparatels they set in an integrated manner in the normal organı m Thrs 18 best illustrated in Tig 3 vluch gl es an idea of hon both forces act simultaneously one supporting the other in draning blood tos ard the heart The question arises now as to the relative contribution of these frontal factors ind the 2 is a tergo in venous return It is doubtful of this question can ever be 394aered precielt In & circularl arranged distensible and collapsible fud filled s tem in which the fluid is kept in motion by two forces one pushing and one pulisng ·111 EVOLS RITURS it is difficult to assess which force is the grcater one at a b11cn point in the circle The vis a fronte created by both the inspiratory and ventricular muscle contrac tion low crs atrial pressure and thereby increases the pressure gradient between the capillaries and the heart Lien a small decrease of atrial pressure can be capected to have a great effect on flox bccau e of the low resistance in the seno atrial inflow tract as compared to the high rcsi tance encountered in the arteriolar and capıllary bed llon much this lowering of atrial pressure could promote flow in the absence of 1218 a tergo would not be c24 to as ( under physiologi cal conditions How cver it appears tlint the pres ure gradient between the cap illurics and the right he art is created by the concertad action of both forces tlıc 218 a tergo which is manly rc ponsible for the height of capillary pressure and the 21s a fronte which is mainly responsible for louering the lciel of the right atral pressure Both forces work togetlier for the return flow of blood Summart ing The lieart assumes a relatively cos creign po ition concerning venous return by actively ladling blood from the scnous ci tern in accordance with its avail ability for the next ejection Thic ventricular contiaction wutomatically assures a coordination of the amount of inflow and ejection The pliable central veins form 1 collap e chamber sluch as ures the transformation of teady flow from the tissues into discontinuous flow for the filling of the heart The collapse chamber is the scnous counterpart of the compression chamber Atrial contrac tion stop atrial inflow and cicates a large central venous reservoir available for rapid atrial filling through the next ventricular contraction The vis a fronte created by the myocardial and in pir itory muscles is integrated in the normal organism The ris a fronte appears to be mainly je ponsible for low cring the level of atrial pressure whereas the zis a tergo is respon ible for the height of the capıllary pressure the combined action of both creates tlic pre sure gradient necessary for the return flow of blood ·X Venous Hemodynamics of Cardiac Valve Lesions It obxous that the normal cardiac ariations in dous return are altered by changes in the dynamics of the heart in thta respect the changes produced by le rons of the atrioventrcular stics and perscardial tampon.de ere of particulur interct ance their surgical correction has become very promising in recent scars Unfortunately our inforination on senous return in the presence of valvular defects and or pericardial tamponade is not set based on quantita ne mea urements of phasic for but is predominant}s derived from indirect Aidence of pre sure determinations This discu sion mut therefore be limited to a bruci rowen of ac cral factors concerned with the change of venous flon dynamics in the presence of the elusions It is not intended as a review of the hemodynamics of all als ular delects a subscot slucha is exten rely covered in other accounts by Harnson (1931) Lu ada 199-41 and Haggers (19.2 1951) VITRAL AND Terce Pro WFFICIESCIE'S It is well known that the circulation can be dequutely maintained in pure moutral or tricuspid insufficiencies of moderate degrce (Gorlın et al 1902 Barger et al 1932) Regurgitation docs not appear to be a great as one might Capoet from the extent of the anatomical le son The strigung hemodynamic que tion anzees Why is not the entire intricular volunie of blood regurgitated through the open cntricular orifice into the los pre cure system of the atria and I cans? The amount of blood that is rigurgitated during rentricular systole appears to be limited by the combined action of (teral factors Four of the e should be pointed out here 1 In cxpcrimentally produced mitml and tricuspid insufficiencies only a neg higible amount of blood 14 regurgitated during the pha e nuch corre ponds to the onsetrie ventricular contraction of the normal bicart Dunng tinis pha e a sufficantly high intraventricular pressure is ertated for opening the semi Lunar values and subsequent cjection of part of the blood into the high pressure system of the arteries Back flow into the atria and veins is not appreciable until the beginning of the ssstolic cicction phase (W166ers and Fel 1922 Little 1948) It can be demonstrated in pliysical models that tht amount of back flow during 190metric contraction eems to depend upon the rate at which pressure dexclopa in thic ventricle (ll 190,488 and fol 1922 llibers 1932 Lichau 1934 1933) If a sudden pressure rise as created by compris ing a flud filled rubber balloon the amount of fud de placement from the balloon into adjoining open bottles is relats els mall This sudden comprison would corrcspond to the scometre Sintricular contraction Tecordms to this analogue sudden sentricular con traction may des clop enough pressure to open the aortic valcs without an Il ·116 VENOUS RETURN appreciable fluid displacement from the ventricle into the atrium On the other hand, a slow compression of a rubber balloon will result in a major displace ment of fluid into an adjoining lon pres ure ss.tem (atrium), before sufficient pressure for opening 1 vifve toward an adjoining hiylı pressure systrin (artery) develops 2 During ventricular ejection regurgitation may be impeded by a narrowing of the atrioventricular ring It is beliczed that the contracting ventucular muscle bundles effect this so called muscular contraction of the atrioventricular ring By inserting 1 finger through the atrial appendage one can easily papate the narrowing of the ring during ventricular sy stole Convincing yaual cuidence for the sj stolic narrowing of the mitral ring has becn presented by hantronitz et al (1951) in motion picture of the opened dog licart 3 A partial occlusion of the atrioventricular onfice by the contracting en tricular myocardium is supposed to aid in limiting regurgitation 4 The maintenance of some leaflct inobility limits the ainount of back flow Vobile leaflcts permut by their valic action the inflon of 1 larger amount of blood during ventricular dia tole than is rigurgitated during sy stole Tlie rationale of several procedures for the surgical correction of mitral insufficiencies is based on the remuning mobility of the computent leaflet llarken (t al 1934 Harhen 1935 Bailey 1935 Bailey et al 1905) Durin, li astole these leaflcts forin a large valve aperture which permits adequate ventricu lar filling Honeycr during systole they do not close cufficiently and lonte an aperture of incompetence through wich a jet of blood is cccted back into the atrium Functional competence of the atrioventricular values can bx ? cstablished by merely abolishing the aperture of incompetence This may be accomplislied by various baffles grafts or plicte vluch occlude the aparture (Bailey Jamison et al 1954 Barley 1995 Barley ct al 1935 Harhan et al 19.1 Hirhen 19301 or fy n judicious reduction in the size of the atrioventricu lar ring (Davilla et al 1955 Bailey et al 1951 Benchoux and Chulnot 1971 Immobile leaflets may be suit ibly nobilized prior to the correction of the insufficiency In mitrni and tricuspid insufficiencies atrial pressure riscs during sentneula sy stole due to the regurgitation of the ventricular blood plus the trial inflou froin the veinis The rise of atrial pre surc crentes a lu, atrioventricular pre sure Gradient for the next diastole (Wiggers and I cil 1922 Little 1948) This results in a more rapid and griater filling of the sentricle thrin norinally the ventricle accomodatcs during diastole the regurgitated blood plus the norinal venous return The resulting scntricular dilatation may widen thu atrio en tricular ring and in turn increase the already custing insufficiency of the leaflets As this lcads to greater regurgitation it cstablishes 1 vicious cycle wuch is considered characteristic for the elf aggravating nature of the insufficiencie Partial bloching of the leah alone may therefore re ult in a reduction of the utrios entricular annulus merely by decreasing the ventriculır dilatation (Harhen ct al 1954 Harhcn 1955) Phasic changes of enous return in tricuspid in ufficiency have been directly recorded in the unanesthetized human by Alullcr and Slullingford (1955) Using 1 double lumen Cournand catheter with a differential minopeter they demon ·VENOL > IEVODI VIVICS OF CARDLAC I ALLE LESIO 117 A B) NA SYST | SYST FIGURE 31 Blood flow between the superior vena cava and right atrium in a normal subject (1) an lonc with tricu pid incompetence and high enous pressure (B) (Redrawn from in original record of Vuller and Shillingford 1900) trated directional change of flon in the pre cncc and in the ab ence of a tricu prd in ufficiency Fig oft illustrate uperior caval flon in a normal subject During atrial systole flos was brief rever cd Forward fou reached its maumuin in ventricular y tole topped brick at the end of sy stole and was again accelerated during ventricular diastole The similarity of this flow pattern and tho c obtained in caperimental anım als suggests that fundamentally the ame hemodynamic crcnts determinc venous return in the mammalian heart It hould be pointed out though that the tracings in Fig Jt are not a quantitative measure of flor ince the cro cctional arca of the ve sel was not fixed and an over hoot in both directions could be caused by large fluid columns in the catheters and by the distance between the holes of the catheter (10 cm apurt one in the atrium and the other in the uperior vena cava) In a subject with tricu pid insufficiency flon was rcier ed during ventricular ystole and greatly accelerated during diastole (Fig diB) Surmart ing The normal rapid forward movement of central venous blood during ven tricular y tole is rescrsed in the pre cnce of a large atrio cntricular sale insufficiency Vaumal forward flon occurs under the e circumstanccs during Ventricular dia tole Tigorous ventricular contraction inay produce (nou,lı pre ure in the sentricle to open the aortic al cs without causing an appreciable fluid movement from the sentricle into the atrium through the onfice Narrow ing of the atrioventricular ring and partial occlu ion of the Icah during ven tricular contraction may hinder regurgitation into the atrium In the surgical correction of some insufficiencies one can utilize the maintenance of leaflct mobility which limits the amount of back flow during sentricular sy tolc ·118 LEVOUS RETURV VITRAL AAD TRICI SI ID STOVOSE The great technical difficulties encountered in creating experimentally a mutral or tricuspid stenosis similar to a natural one are in part responsible for the muager know ledge of phasic changes in venous return in the presence of the c lesions (Katz and Siegel, 1931 Opdy he and Brecher, 1951, Hamilton et al, 1954) On the basis of phasically recorded pressures acute mitral stenosis appears to affect enous return as follows Increased resistance to flow offered by the anal! mitral orifice is in part overcome by increased Icft atrial prc sure, more vigorous atral muscle contractions and a prolonged ventricular filling tme Hence a steep left atrioventricular pressure gradient is characteristic for outral stenosis Total systemic and pulmonary venous return arc diminished (hatz and Siegel 1931) Pre sure neasurements in humans rcical particularly that a decrease in the duration of ventricular diastole reduccs ventricular filling The diastolic filling period may be shortened by either an increase in licart rate or a relata e prolongation of intricul ir systolc Thus, in mitral stenosis moderate tachycardia alonc may lead to bouts of pulnionary cdema by backing up of blood in thc pulmonary veins (Gorlin et al 1931) Since mitral stenosis is often associated with some insufficiency (incompetence of the rigid leaficts) regur gitation into the left atrium occurs generally during ventricular systole The amount of regurgitation is again determined by the plı sıcal factors discus ed above The production of an acute interatrial septal defect for the relief of pulmonary enous congestion in intral steno is is without detectable dynamic effect (Op dyke and Brecher 1951) It appears therefore doubtful whether the creation of an interatrial scptal defect would be beneficial for the relief of pulmonary congestion in cases of human mitral stenosis The greatest improvement of venous return is achieved by the surgical cor rection of the stenosed atrioventricular valses (commisurotomy salvuloplasty Talvotomy) In this operation the lies are adequately separated citler by a finger or with the aid of a suitable instrument such as a commissurotomy guillotine or dilator (Cooles and DeBihes 1954 Glos cr, 1904 1935, Olall ct al 1954 Bailey 1957) Much of the vale motion can be restored when the valves are separated at the full length of the commissure Thil commi sur otowy reduces immediately the high atrial pressure It re ults in a significant decrease of the mean diastolic atrioventricular pressure gradient Thi fall appears to parallel the improvement in venous return (Gordon et al 1994 Yu et al 1954) In some respects the lemodynamic cients in tricuspid stenosis are similar to those described for intral stenosis Ferrar et al (1953) found in catheteriza tion studies of a patient with tricuspid stenosis that her atrios cntricular pres sure gradient remained stcep during ventricular diastole Apparently the right i cntricle is filling throughout this entirt period Tle stenosed sali es do not open sufficiently in diastole Hence they present the early inrush of blood into the vcntricle which is so important for normal ventricular filling In pure tri cu pod stenosis right atrial pressure increases very much during atrial sy tole und falls continuously during isometric ventricular contraction and carly in tricular ejection The impediment to schous return bs tricu pid stepo is lends ·TLVOL XOBIVUS OE CARDIAC VALSŁ LISIONS 119 to the well known chacu syndrome of congestive failuri ulitch • beyond the scope of the prc ent discussion Summan ing Elevation of atrial pre urca increases the atrosentriculur pressure gradient in mitral and tricuspid eno (s The sma) orifice proients rapid sentricular fillirg at Carly drastolc mahing the filling niore dependent on the existence of a long diastole Commi surotony of the stenosed atrioventricular akses re ult in an immediate and lasting improvement of venous return PFRICARDIAL EFFt 10 Adrcu sion of circulatory changes re ulting from pericardial ctfusion is included in this chapter because in some hemody nunc re pects thewe changes rescnble those caused by ah ular di orders Pericardial tamponade has often been produced in acute and chronic form in animal experiments by infusing saline solution or other funds into the perirardial sae \erlich 1931 Vietcalfe ft al 1932 Boucchet al 19.2 a) Pre ent knon ledge of thic hemodynamc alterations is masnls dernied froni pressure measurements 11 hen in animal cxperiments involving the acute form the perirardial sac is progressuiely filled with alıne venous return is at fir d impaired only during ventricular diastolc since the pericardial tamponade hinders the expansion of the atrosentricular cavity llence the strohe volume becomes smaller Ten tricular ejection decreases the pericardial pre urc and by reducing the impeda ment to atrial filling creates a more favorablc veno atrial pressure gradient (Verlich, 1951) Further progression of the tamponadc diminishes venous re turn not only during diastole but also during ventricular sy stolc since atrial info is impeded When the sono atrial gradient becomes diminished during ventricular sy stolc a self perpetuating cycle appears to develop Nerlich suggests that the decrcase of the systolic discharge reduces the facilitating effect of Icntricular systole hercupon the reno atrial pressure gradient becomes less favorablc This in turn diminishes y entricular filling and so forth When this phase is reached venous pressurcs tise and arterial pressures fall abruptly Finalls with further effusion all intravascular pressures approach the same value of about 20 mm Hg shrn the heart ccascs to pump blood cliectively from the venous to the arterial side (Metcalfe et al 1912) The acute tamponado affects blood inton into the right heart about to the same catent 29 it does infony into the left heart Chronic experimental constrictise pericarditis in dogs to develop in such a manner that it mtcrferes with the return flow of blood more on one side of the heart than on the other If the tamponade primariiz blocks luft heart filling it results in the development of pulmonary eduini and a marked increase in blood solume In such case systeinic venous pre sure does not n e significantly and a cites fails to desclop On the other hand of the right inflon tract is primarly affected systemic venous pressure rists and hind leg edema der clops but pulmonary edema and changes in blood volume do not occur (Boucck ct al 1952a) These two different types of circulatory failure can also be produced without pericardial inyolsement by constricting separately the pulmonary se ·120 TEVOUS RETURN nous infiou tract and the vena cala inflou tract to the heart (Boucсh ct al 1952b) In chronic espermental pericarditis the tamponade is relieved by a pericardial ic ection which inust include the area of the pericardium overlying the inflow tricts It appears therefore that the pricardial tamponade acts primarily by restricting enous return at the inflou tracts of the heart The ch iracteristic low cirdic output is the result of the rc tuction in ycnous return Pre suri tracings from the right atrium and ventricle in patients with chronic constrictne pericarditis before and after pericardicctomy seem to indicate that in pericarditis the systolic ejection of the heart is relaticly less impaued than the diastolic filling (Ilanscn ct al 1931) Early diastolic ventricular pressure in patients with pericarditis varics little from normal On account of the steep atrioventricular pressure gradient thc ventricle begins to fill rapidly in carly drastole but is limited in its further filling by the pericardial constriction This causes a marked nic ofend diastolie ventricular pre sure which is typical for these patients Shortcoin, of the diastole by licart rate acceleration is fairly well tolerated becrusc ventricular filling is funited any how to carly diastolc under these conditions Summan ang Pericardial tamponade reduccs prinarily ventricular diastolic filling Since the ventricle cinnot eject without filling the lost output is the most character istic effect of pericidial cffusion Predominance in the construction of the Icft atrial inflou tract causes circulatory failure associated with pulmonary cdema, whereas that of right atrial infloss tract leads to failure associated with ascites ·XI Venous Return During Cardiac Surgery From the considerations in the previous chapters it may be conciuded that the combined action of anesthe 13 and open thoracotomy diminishes the cir culatory reserve This can be accounted for bx (1) a decrease in the pulmonary blood depot (2) heart shrinhage (3) the ab ence of thc re piratory pump and (4) an increase in pulmonary bed resi tance plu a tamponade of the licart and great cssels by positive pres ure lung inflation Hence additional interference with vcnous return by cardiac surgery may result in further reduction of the narrowed circulntory safety margin Thus a brief account of some factors in fluencing cnous return in cardiac surgers may not be miss It is not intended to consider here the effect of all heart operations on venous blood flow but rather to call attention to the application of some of the hemo dynamic principles presented in the previous chapters For comprehensive re Views of the rapidly developing field of cardiovascular surgery reference is made to the International Symposium on Cardios a cular Surgery held at the Henry Ford Ilospital in 1993 (report cdited by Lu 19))) and the recent textbook on Surgery of the Heart by Bailcy (1993) During intracardınc surgery a number of methods are currently emploved which may be divided into two gencral groups closed heart and open heart surgery In closcd hcart procedures the operative field within the heart is not directly visible in these cases the heart and great vessels remain filled with blood and the operating finger or instruments are introduced through a suit able mcision in the wall of the atriuin ventricle or ve sel In open heart surgery the heart or adjoining vessels are briefly blocked off from the circulation bv an occlusion of the systemie veins This permite direct vision of the operative field when the heart or ve sels are opened and drained of blood In cither group it is essential to pcrfu adequick tlic coronary cssels and brain during the relativ cly hort period when the urgical procedures are car ried out within the heart Temporary blocking or interfcrence with venous return as ucl does not seem to be of major detriment to the organisin as long as by some ineuns or other sufficient nourishment of the myocardium central nervous system and kidneys is assured In cloud heart surgery this must be assured by minimal embarrassment of the returning blood which after its ow genation in the pitzent s lungs is cjected in a normal muner by the contraction of the sch tricular muscle On the other liand in open heart surgery the same goul must be reached by direct perfusion of the arterial system under high pressure with oxygenated blood In this case it does not matter in principle whether the per fusing blood is taken from an infusion bottle or taken from the patient s icins and then used for perfu son after it has been collected and oxygenated 191 ·122 TENOUS RETURY CLOSED HILART SURGERY In closed heart surgery venous return is mainly interfered with when the ex ploring finger and/or operating instruments are pushed into pathologically narrowed parts of tht inflow or outflow tract This may be illustrated by the situation prevailing in the mitral or tricuspid stenosis In an operation for a lesion of this type the finger is inserted either alone or together with a guillotine knife or dilator into the atrium through an incision in the atrial appendage or wall (Gloucr 1934 19) Dubot 1959) The insertion into the atrium in it self does not appear to binder cardiac inflow Only the introduction of the finger and instrument into the mitral or tricu pid orifice for the purpose of separating the valve leaflets blocks ventricular filling Dubot (1955) has de cloped a special mitral dilator w lich he also used for tricuspid and pulmonary steno es Manipulations can be carried out very fast with this instrument He points out that due to the specd attained with the dilator the atrioventricular orifice is only obturated for tho or thrce leartbeats In most cases of closed heart surgery the actual operative procedures at the site of the lesions are of relatncly short duration By a suitable release of the instruinental inflow impediment the surgcon can usually control venous return sufficiently to permit the development of adequate arterial pressure and flox If this cannot be attained an intra arterial infusion of blood is given during the critical period when the return flow of blood is greatly reduced Especially interesting from a hemodynamic viewpoint arc the interatrial septal defects and their surgical repair These defects are the inost common cardiac anomalies of congenital origin In the presence of a defect in the septum between the two atrıı oxygenated blood may be shunted from the left atrium into the right atrium and unoxygenated blood may be shunted from the right to the left atrium The direction of the shunt flon depends upon the prevailing pre sure gradient between the two atria The gradient varies in magnitude and may reverse its direction during the cardiac and respiratory cycle (Brecher and Opdyhe 1900 Shaffer et al 1954) Due to the higher volume clasticity coeffi cient of the left atrial walls the mean pressure is higher in the left than in the right atriuin (Little 1949) Therefore more blood is usually shunted from the left to the right atrium than in the oppo ite direction The shunted blood may greatly increase venous return to the right ventricle This puts an extra load on the right ventricle which has to cject the normally returning venous blood plus the shunted blood When the right ventricle fails to discharge the large amounts of inrushing blood the pressures rise in the right atrium Thercupon the shunt flow will reverse its direction and blood wall pass from the right to the left atrium Tlus may relicse the strain on the right ventricle (Brecher and Opdyke 1931) Thus the creation of an interatrial septal defect may relieve the right sentricle in conditions which cause a lugh resistance in the pulmonary bed (Leeds et al 1955) Various methods have been de cloped for å repair of interatrial septal de fects I cnous return inust not be embarrassed as a result of these procedures The choice of the method depends to a great deal upon the size and location of the defect and pathological changes of the outer atrial wall Bailey et al (1953) and Bailey (1995) des cloped the atrioseptopexy by which part of the pathologi ·EVOLS KITLRS DURING CARDIAC SURGER) 123 cally enlised right atrial » all 15 u cd in order to cover the hole in the septum The rationale of this mcthod is the use of an encess of cardiova cular ti sue in tlıc form of the u ually distended right atrial wall for cocring a lach of cardio vascular tus uc in the cptum (rapres ed by the defect) This method such con cries the atrial wall has the advantage of not restricting venous return from the caval vcins Sondergaard Bjork and Crawford (ce Lam 1950) u e thic circumclusion operation by which uitably located defccts can be drawn together with a ligature The ligature is pe ed bluntly around the defcet area through a clessage linc lctween the muscle layers of the two atria The pro cudure is relatively smple Night and leſt atria retain their hape and the inflow tracts to the heart irc not bloched Hemodynamically intere ting is the atrial vell operation by Cros and his colleagues (1993) and Cross and Watkins (1933) The r authors utilize the fact that the sens rcprc ent a low pressure ny ten. They sell 2 oft rubber funnel to the right atrial wall incrc the wall and permit the blood to rise in this well Right ventricular filling appears to be normal de pite the wide open atriun The repair of the atrial septal defect is made «recth (though not by direct non) through the large wall opching Usually blood rises only a few centincters in the well in accordance with the existing atrial pressure Honever if tricuspid regurgitation is as ociated with the interatrial septal defect atrial pre sures have been found to risc o lugh that the well could not be applıcd (Watkins and Gross 1957) Summar ing In closed heart surgers venous return is usually blocked for short periods by tic insertion of the operating finger and instruipent in the narrowed passages of tlıc inflow or outflow tracts The brief duration of the interference is generally Wull tolerated In interatral septal defects return flow to the right sentricle 15 increa ed by the predominance of shunt flow from the left to the right atrium In the repair of interatrial scptal de fects particular care must be taken not to restrict caval inflos OPEN HEART SURGERY Two methods hypothermia and extracorporcal circulation have beca Succe fully employed to permut intracardiac surgery under direct vision They can be u cd alone or in combination with one another In hy pothermia the organi in is suitably cooled to trmperatures ranging be tween 28 und 30 C in order to reduce the metabolic needs of the tissues es pecially thosc of the nervous system and myocardium Iccording to Berne (1954) livpothermia as employed in cardiac surgery docs not seriously interfere with my ocardial competence as such provided the natural slow rhythm or the heart is maintained By ineans of an arterial infusion of oxygenated blood the vital organs can bc idequately supplied with oxygen during the critical Period uhen the heart is open In order to enter thc lieart the caval cins and the azygos vein are clamped Surgical mancui ers may thus be performed under direct vision on the right heart for periods lasting from Y to 20 minutes (Bules Cookson et al 1994) When hypothermia alone is used (without the ·124 I EVOLS RETUR addition of an extrncorpoic al circulation or arterial blood infu non) the safe period of inflow st1 is is limited to about 12 minutes (Gollan ct al 190pThe marhed congestion in the ste nuc sens as such docs not appear to have a detrimental (ffect on the tis ues (Tor u discussion on du antiges ind di ad vant iges of various methods of inducing hypothermia sc Lim 19 p 108 ) Extracorporeal circulation has been employed in variou forms to bypas parts of heart and great els or the entire he art If the bicart is completely bypassed the cardiic chambers can be opencil and intrac udiac operations such as repair of an interatral or interventricular septil defect can be performed under direct vi ion in a relatively dry field The effectue working tune within the heart cin thereby be incrt ised to 20 or 30 minute For bupas ing the heart I illchei and his co workers (1990 sec il o for pre vious literature) base de cloped a method of controlled crocirculation which has proved to be very successful for the intracardiac surgery of normothermic patients In cross circulation blood is continuou ly circulated through tulcs from one subject to another and back again Uncontrolled cross circulntion has been described by Lgdahl (1905) In applying the principle of controlled cro cuculation to cardiac urgery one subject serves 19 donor and the other is the patient Blood from the brachial artery of the ane thctized donor i pas cd through tubing va finger pump (gmamotor pumpl to the aort 1 of the pa tient It perfuses tlic coronary arteries and other vital organ After pinge through the patients capillary beds the blood is collected from the uperior und mferior caval veins and returned through tubing with the aid of a pump to the donor s veins After the cro » circulation his started the right trial in ion to the patient s heart is stopped by clamping the cutaf veins and 9 eurde otomy can be performed for direct vision surgery It is obvious that such a system mu t be o balanced that exactly the une quantity of blood flows from donor to patient as from patient to donor Fluctur tions in the patients inous return (pecially may unbalance the tem If less blood is returned from the patient to the donor than is pumped from the donor to the patient the anesthetized donor may become unnotic bly (11n guinated Hence the detection and immediate corrcetion of differences in the two way flow is an important problem which must be solved before (10 lation can be generally applied with reasonable safety In our laborators we became recently interested in this problem and scarched for a method of balancing the two way flow in cro s circulation (Brecher et al 1955) In ninal cxperiments cross cu culation flou both ways vis simultant ously mca ured with two bristle flow meters (see Fig 15} 4 difference in the flow rates indicated an imbalance of the flon from donor to recipient and vicc ver a Thuis method appear lower cr rather complicated for use in the operating 1001 Since the cardinal probletni a prevention of the donor s unnoticed blood loss we u od the donor as a cumulatic flow meter' by placing him during the entire cross circulation procedure on zero reading scale Tlus inflow and outflow from the donor could be continuously monitored Blooit loss from the donor could be accurately measured and icplaced by intras cnous mfusion The a permental arrangement for cross circulation with the aid of donor a scales is illustrated in Fig J5 It appears that the u c of scales cols es simply and ic circil ·I EVOLNI TLRT DURING CARDIAC SLRGERY 12) DONOR DONOR SCALES FEM VEIN FEM ART w SOS RECIPIENT PUMP AORTA ri VENAE CAVAE INFUSION BOTTLE CONSTANT VACUUM RESERVOIR GT RED Diagram of controlled donor cross-circulation The two was lood flow from donor to recipient and Ice crsa is balanced with the aid of su] on naich the donor is resting Suction from the re-croir on the caval seins of the recipient is kept mill 15 oder to forstall nous collapse curately the problem of regulatin, the tuo mar blood flow during cross circu lation under operating room condition The fluctuations in vous return from the patient during cross circulation urther unpredictable It has been ob erved in dogs and to a le er degree in humans that the arterial blood pres ure falls in the patient shortis after cross circulation las stirted similar obscriations reported by Dodrill and his asso crate (1932) during a bypass of the right heart suggest that this phenomenon Inight be cyplainable on a reflcı banks ( inierse Bainbridge reflex) The re moval of the normal diston ion of the atrium and breat sens by the suction of the pump would initiate reflewy a lowing of the heart and a decrease in blood pre urd by generalized vasodilatation Apparent's owing to neurogenie or cliemogenic fluctuations in the patients Tenomotor activity blood 1, sometimes pooled in the peripheral parts of the nous y tem during the course of tlie cross circulation when this occurs or the patient loses blood during the cardiotoniy the pump cannot remove enough blood froin the patients veins and the two wa fion of thic cross circulation be conxes unbalanced In order to make the venous blood fou to the donor in dependent of fluctuation in the necipients 1 epous return we found it best to drain the recipients blood into a uitable re crror Trom there it is pumped at a con tant flou rate to the donor The Te cri or is indicated in the lon cr center of Fig 13 Thic iginamotor punip which is generally used for cro s circulation doi clois ·126 VENOUS RETURY a cry lugli degree of suction If the cannulac from the casal veins of the patient lcad directly to the pump it may happen that the caval veins collap c completely or intermittently during fluctuations of the patients scnous return Because in collapuble structures flow decrcascy with extreme degrees of suction (sce Fig 20), le s blood is returned after cai al collapse sia pump to the donor The com plete closure of the phable y enous vall over the holes in the collecting cannulae may dumage the car le and may cv en create 1 vacuum in the tubing bctucen the patients i cins and pump leading to a degassing and gas bubble formation in the blood It was found that the interpo ition of a resers or avoids these difficulties If no reservoir is used judicious blood infusion into the patients veins helps to present the onset of collapse and keeps the caval fon constant At any rate, with or without ieser or the degree of suction should be so ad justed that the patient's coval veins deplcte optimally without entering the collapsed stage Using as a guide curic 4 of Fig 2) it is best to sorh at the highest portion of the curve before it flattens and declines to the right Blood pooling in the patient s veins can also be favorably counteracted by the use of mild vasoconstrictor drugs The amount of blood necessary to perfuse the vital organs during cros circu lation is far less than the patient s cardiac output Andreason and lat on (1952) and Cohen and Lillcher (1954) found that in dogs the needed amount cor responds approximately to the voluinc flow through the azygos vein (one tenth of the cardınc output) when the cas al veins are clamped The term azygos factor has been introduced to characterize this amount The important factor responsible for the success of open vision intracardiac surgery is the low rate of volume flow which has been found sufficient to keep the anesthetized normo thuimc patient alive (about 12 to 25 per cent of the resting cardiac output) The function of the donor in controlled cross circulation is to oxygenate blood for the perfusion of the patient whose heart and lungs are by passed Since there is always an element of danger in olied for the donor the future development of oprn cardiac surgery is directed toward a replacement of the donor by equip ment for blood oxygenation The tcam working with Lilleher has again been leading in this direction Campbell ct 11 (1955) developed in animal experiments a ratheı simple method substituting for the donor an isolated dog lung Following this work heterologous lungs have been successfully used by Lillehci and also other sur geons for by passing the heart and lung in patients during open vision cardiotomy 11 arden et al (1995) (seo al o Lillehci et al 1935) des cloped 1 till sampler technique of perfusing child patients from a reservoir of previously collected arterialized venous blood 'By warining the arm of a blood donor local arterio enous anastomoses are opened whereby the oxygen content of the collected venous blood is greatly increased During the perfusion of the patient the blood returning from the patient s caval veins is collected via a pump, in bottles It one could reoxygenate this blood in a simple manner within a reasonable period one could use it again for the perfusion of the patient and thereby hcep the amount of pre collected blood relatively small work on the development of 2 suitable 'bottle oxygenator is in progress It has been u ed successfully in 17 patients by hay and Cross (1956) ·VEYOUS RETURY DURIYG CARDIIC SURGERY 137 Looking back on the developnent of the various nicthods of extra corporeal circulation for by pusing the heart and lungs it appears that the cycle of de velopment is coming to a close with perfusion of the patient from bottles and re oxygenation of the patients blood in the collection bottle The perfusion bottle and re ou genation bottle arc cssentially a implified 1 ersion of the more complicated pump) owy genitors (arnfical heart lung! (Scr Jongbloed 1951 Clones et al 1951 hus crow 1933 Velro c 1935 Hayes et al 1903 hirklın it al, 1933, emunct 1! 1932 Dodrill et al 1955 | Duc to the fact that the tcclinical dev clopment of the pump ou genators ils not set sufficiently ad anced for anfc intracardiac open usion surgers Lillche and his co workers developed the controlled donor cross circulation which will probably be re placed by the simpler bottle methods Under all conditions whether cross circulation an i plated lung artcrialized renous blood or pump ovy genator are used due consideration should be given to the laws of the collapsible tubes when the patient s venous blood is collected Sunmari ing In open cardiac surgery under hypothermia the warhed schous distension by bached up blood does not appear to have detrimental effects as long as the low crcd metabolic nccds of the ti sues are taken care of In controlled cro circulation for direct vision intracardiac surgery blood fton must be accurately bulanced in both direction from the donor to the patient and vice versa Balancing can be qu used by placing the donor on ciles during the operation Fluctuations in venous return from the patient may cause complete collapse of the venae cavae if the suction appplied as excessic The collapse of the pa tichts vena cava by strong suction should also be avoided in other techniques of extra corporcal circulation ·Final Remarks In considering the various factors hich are responsible for the return flow of blood to the heart one may feel tempted to cvaluate the importance of cach factor on a percentage basis In doing so one would soon discover that, cxcept for the cjecting force of the ventricles, cach individual factor could be eliminated without altering appreciably the quantity of the returning blood and cardiac output However it would be fallacious to conclude from this observation that all factors but ventricular ejection are unimportant This may be illustrated by the following cxample hagan (1932) destroyed 70 to 80 per cent of the outer wall of the right ventricle by cauterization and discovered that the right heart still possessed a nearly normal compensatory action when the pulmonary artery was greatly constricted Venous prcs ures and apparently venous return were not altered after the cauterization Recent investigations have been interpreted as showing that the maintenance of the practieally unimpaned function of the mght heart must be attributed to the un de troy cd portions of the inyocardium (Rose ct al 1959) It would certainly be crroncous to deduce from the cauterization cyperiments that 80 per cent of the right ventricular wall is unmportant They only cm phasized the fact that the heart possesses remurhable reserve powers These arc important physiological factors of safety as succinctly pointed out in an editorial articlc by Alexander ind liggers (1993) The factor of safety, a term used in engineering indicates the margin by which the strength of matcrial or struc turc cxceeds the actual working stress to which it is submitted in normal use According to this concept the various components which norinally contribute to the return flow of blood to the heart should also be looked upon in their en tirety as essential factors of safety The combination and integrated action of all factors--the ventricular ejection the re piratory pump the su tolic in tricular attraction the recently demonstrated diastolic ventricular suction the muscle pump and venomotor activity-widen the margin of safety thuch assures the adequacy of venous return under normal and abnormal conditions 198 ·Bibliography IL LAVER R S 19181 Strain gauge In Method in Vedical Research Chicago I car Book Publishers Vol 1 po 191$b In vivo ob ervations on distensibility of the femoral enous system Prou Soc Larer Biol Ved 6 410 1901 Influcnce of the diaphragm upon portal blood flow ind cnous cturn im J Physiol 16739 W WIGRY CJ 1933 Cardiac fuctor of safets Circulation Re cauch 1 99 EDWARD WS AND IRENE JI 193 The di tensibility character tics of the portal vascular bed Circulation Reseuch 1 2.1 10311 The influence of constrictor druge on the distensibility of tlc splanchnic 1 enous system analyzed on the basis of an aortic model Circulation Research o 140 1951b Tlic participation of the cnomotor system in pressure reflexes Circulation Rc earch 2 103 1950 Venomotor tone in hemori bage and shoch Circulation Rescarch 3 181 1956 Reflex alterations in vcnomotor tonc pro luced by vcnous congestion Circula tion Research 4 49 ANDREASEN IT AND W4150 I 1932 Experimental curlio iscular surger Brit J Surg 39 518 ANKEVES JL HLBAY C A HACKETT P R AND IIIyoso RA 1004 The effect of po atave an i negine pressure re piration on unilateral pulmonir blood flow in the open chc Sug Gioce (OL E OS 600 AISILTZ F DELHEL B DRLBE IC AND SEUSING J 1900 Uber die Bedeutung des intra pulmonalea Druckcs les der endotrachealen Beatmung Der Inaesthetist 2 ADRA G V AND WHAT DG 1934 35 mm cine camera incorporating a I luullips ray image intensifier J I hy siol 1? 1P A CHER AND SPLKGEO W 1919 Compression test on aqueous icing of glau comatous eyes aj plication of hydro ly namie principles to the problem of intraocular fluid elumination Am J Ophth 99 229 Aschoft J 1907 Marmeubergang an tromen les Blut Irel f ges 1 łysiol "es 264 -- AND EVER R 19,6 Die Funktionsweise der Duathermie Thermo-Stromulir Ireb Il ges Phy jol of 133 AVIADO D M JE AND SCIWIDT C F 1903 Reflexes from stretch receptors in blood vessels hcart and lungs Phi rol Res 30 21" BAILEY C P BOLTO II C JAVISOY W I AND NEPTUVE H B 1933 Itrioscpto pexy for interatrial septal defects J Thors le Surg 06 181 Cookso B | Dow VING D F AD \EPTUE 1 B 1951 Cardiac surgery under 1 spotlemia J Thoracic Surg 7 13 JASON W L B EST A BOLTON UE VicUOLS I T AND GEMEIVII 4XDT 1 1934 The surgical orrection of mitral insufficiency by the use of pericardial grafts J Thoracic Surg 531 1955 Suikers of the Icart 1 hiladelphia Lea & Febiger Baltos HE JAVISON WL MICIIOLS II T AND LIKUFF # 1995 Niethods of surgical treatment for alvular a sufficiency of the beart In International Sympo ium on Cardio, ascular Surgers Philadelphia an i London WB Saunders Co p 392 BARGER & C Rot B B AND RICHARDSON GS 190? Relation of valvular le sons and of excrci e to auricular pressure work tolerance and to des elopment of chronic con gestise failure a dogs im J l hy siol 109 384 BARRI D 18 6 Experimental researches on the influence exercised by atmospheric pres ure upon the progression of the blood in the icons upon that function called abors tion and upon the presention and cure of the symptoms caused by the bitcs of atilor 199 ·130 VENOUS RETURN AND renomous animals London T and G Underwood (quoted from A Monograph on Veins Franklin 1937) BAXTER I GAD PEARSE J W 1931 Simultaneous measurement of pulmonary arterial flow and pressure using condensor manometers J Physiol 115 410 BEECHIER HKBEX VET HIS AND BASSET D L 1913 Circulatory effects of sacreased pressure in the airway Anesthesiology 4 612 Bexicon RAD CILALAOT P 1935 A method for the surgical correction of mitral insufficiency J Thoracic Surg 80 148 BENNINGHOFF A 1935 Anatomische Grundlagen der Beziehungen yon Atmung und Kreislauf Nauheim Fortbildungslehrgang Vol 11 (quoted by Bohme 19 6) BERGMANN G 1938 Strombor te ein elchtrischer Geschwindigkeitsmesser fur Ilussigkeiten (2 Vitteilung) Stromhanule und clehtrische Messanordnung Ztschr f Biol 93 536 BERSE R M 1954 Vyocardial function in ses ere hypothermia Circulation Re earch 90 BETTICIIER | MAILLARD J AND MULLER A 1951 Un manometre differential a transmission clectrique entitrement alimente sur le reseau alternatif pour mesurer la vitesse decoulement dans des tuyaux et des vaisscaux sanguins Helict physiol ct pharmacol acta 12 112 BLAIR HI 4 AND WEDD 1 M 1916 The action of cardiac ejection on enous return im J Physiol 140 528 BLOOMFIELD R. 1945 Simultancous registration of intrathoracic right intracardiac and systemic pressure in man Proc Soc Exper Biol & Med 60 5 BONNE 1936 Uber den ahtis en Anteil des Herzens an der Forderung des Teacnblutes Ergebn d Physiol 33 251 BOUCEK RJ GRINDLAS J HAND BURCUIELL II B 1932a Experimental constrictive peri carditis analysis of induced circulatory failure Im J Physiol 109 434 1952b Experimental constriction of inflow tracts in the heart analysis of circulatory failure Am J Physiol 109 41? B01D T E AND PATRAS M C 1911 Variations in filling and output of the scntricles with the phases of respiration Im J Physiol 134 74 BRAUER L 1904 Untersuchungen am Herzen kongr inn Med Leipzig (quoted by Eb stein 1901) BRECHIER G 1 AND OPD) LE DI 1930 Effect of normal and abnormal respiration on hemodynamics of experimental interatrial septal defects Am J Physiol 16" 507 AND RITTER E R 1931 An optically recording tambour flowmeter and a compensator for large volume blood flow Rey Scient Instruments 62 1018 AND OPD KE D F 1931 The relief of acute right sentracular strain by the pro duction of an interatrial septal defect Circulation 4 416 1952 Vechanism of venous flow under different degrees of aspiration Am J Physiol 109 423 MIXTER GJR AND SIIARE I 19.2 Dynamics of vcnous collapse in superior vena cay 1 sistem Am J Physiol 171 191 AD MIXTER G JR 1992 Augmentation of venous return by respiratory efforts under normal and abnormal conditions Am J Physiol 171 710 1953 Effect of respiratory movements on superior cava flow under normal and abnormal conditions Am J Physiol 1-2 4-7 1903 Venous return during intermittent positive-negative pressure re piration stud ied with a new catheter flow meter Am J Physiol 174 -99 4WD PRACLIY J 1993 A modified bristle flowmeter for measuring phasic blood flow I roc Soc Exper Biol & Med 83 155 1954 Cardiac variations in senous return studied with a new bristle flow meter Am J Physiol 16 423 AVD HUBAT CA 1994 A new method for direct recording of cardiac output I'roc Soc Exper Biol & Ved $6 461 AD 1935 Pulmonary blood flow and senous return during spontancous respiration Circulation Research s 210 REY DYAN NV FIER M BROFWAY B L AND F&EEN RS 1952 Regulation of AD ·BIBLIOGR 4PITY 131 blood flow in cross circulation for intracardiac surgery I roc Soc Exper Biol & Med 89 134 AND HUBAY C 4 1936 enous return and cardiac output during controlled respira tion (Unpublished data) 196 Lapenmental evidence of ventricular diastolic suction Circulation Re earch 4 Sept (la press) BRUBACU IF 1917 Some laboratory applications of low friction properties of the dr hy podcmic syringe Rer Scient Instruments 18 363 Brucke E18,2 Vorlesungen uber Physiologie Hien Tol 1 (quoted by Bobme 1936) BURCII GE COM A E AND AEUMANN C 191% A study by quantitative methods of the spontaneous saritions in volume of the finger tip toe top and postero superior portion of the piana of resting normal white adults Am J Physiol 1 0 433 1950 A Primer on Venous Pressure Philadelphia Les & Febig r 194 Digital Plethysmography New lock Grude & Stratton BURTOV A CAND I ANADAS 1951 Relation between blood pressure and flow in the human forearm J Appl Physiol 4 399 1954 Relation of structure to function of the tissues of the wall of blood vessels Physiol Rev 34 619 EORTOV-Opitz R 1902 I low of the blood in the external jugular e im J Physal 435 CAMPBELL GS CRISP N# JR AND BROWN E B JR 1905 Maintenance of respiratory function with ssolated lung lobes during cardige inflos occlusion Proc Soc Exper Biol & Med 88 90 CARR DT AND Essex E 1946 Certain effects of po tive pre sure re puration on circulatory and respiratory systems Am Heart J 81 53 (ARSON J 180 On the clasticity of the lungs Philos Trans 110 29 (quoted from 4 Monograph on Veins Franklin 1937) CERADIVI J 18. Ztschr Ges Arzte Wien (quoted by Rollet 1880) CHAUVEAU BERTOLLS AND LAROYENNE 1860 J de la Physiol 3 69) (quoted by Rollet 1890) CCNOLIV I 1954 Contributo roentgenchimographico alla dottrina dell attavita diastolica Foha rardiol 13 24 Clowes G H IR NEVILLE WE HOPKINS A INZOLA J AND SIMEOVE FA 1954 Factors contributing to succe-s or failure in the use of a pump oxygenator for complete by pass of the heart and lung experimental and climcal Surgery S6 57 COHEM AND ILLEME CW 1954 A quantitative study of the azygos factor during vena caval occlusion in the dog Surg Gynec & Obst 98 229 COLERIDCE C G AND LINDEN R J 1974 The mea urement of effectxe atrial pre sure J Physiol 196 01 COOLEY D A AND DE BAKEY M E 1954 Surgical treatment of mitral and aortie steno es results of one hundred fifteen alı otomies JAMA 155 2 5 COTTON F S 1934 Does the ventricle exert a suction action in diastole? Am J Physiol 107 168 CRUM J N 1904 An electronic fowmeter for measurement of plasic blood flow Cles cland Ohio Cace Institate of Technology Master of Science The 19 CYBULSKI N 1883 Die Bestimmung der Stromgeschwindigkeit des Blutes in den Gefpasen mit dem neuen Apparat Photohamatochometer Arch f d ges Physiol 37 382 DAVILA JC GŁOSER R 1 TROUT RG MANSURE FS WOOD NE JANTOV O HAND IAIA B D 1955 Circumferential suture of the mitral ring J Thoracic Surg 80 31 DE BURCH DALY I 1996 Blood elo ity recorder J Physiol 61 21 DE JAGER J 1883 Uber die Saugkraft des Herz ns Arch fd ges Phy 8101 0 491 DEVISOV IB SPENCER M P AND GREEN HD 1935 A square wale electromagnetic flow meter for application to intact blood vessels Circulation Research 9 9 DEPPE B AND LETTERER E 1939 Vergleichende tierexp nmentelle Untersuchungen zur physikalischen Schlag olumenbe timmung (1 Mitteilung) Ztschr f Biol 99 07 1910 Untersuchungen uber die Beziehungen zwischen Druck und Strom tarke in hreislauf des Ain Ztschr f Bio! 100 37 AND ·132 1 EXOUS RETURV 4WD AND -AND- DODRILL F D IIILL L AWD GEEISCH R 19,2 Some physiological aspects of the artificial heart problem J Thoracic Surg 2, 133 LUI A NYBOFR J RIPPINGILLE LI AND HUGHE CH 1935 The arterializa tion oi blood is it applies to the mechanical heartlung apparatus J Thoracic Surg 30 608 DONDERS TC 1859 Physiologie des Venst hen Leipzig Inzel DOT C 1993 Method of struinental dilatation la International Symposium on Cardiou ascular Surgery Thiladelphia and London B Stunders Co p 206 DLOVARCO JIRAN RAND NICARTE P 1914 La presion intraubdominal y la pre 1on en la vani cala inferior Reu argent de cardiol 11 273 Reciktu I AD Run R 1911 Influencia de las presiones abdominal y torncıca sobre el retorno icno o en la cara inferior Re: argent de cirdiol 11 256 RECARTE 1 AND RIMIV R 1945 La presion intraabdominal , la regulation del retorno venoso Rex argent de cardiol 11 339 RIMINI RAD RECARTE P 1915 La presion de los troncos nosos del torti Roy argent de cardiol 12 129 AND I REDARI TN 1946 Sobre el estado de di ten joao colapso de las ni caras Estudio radiologico Res argent de cardiol 12 333 —AND SAPRIZA J P 1950 Intento de apreciacion de la pre jou senosa efectiva por medio de la angiocardiografia Rcs argent de cardiol 17 15 AND 1920a Li pression veineuse des membres chez l'homme normal et chez Tinsuffisant cardiaque Compt rend d cong cardiol 3 3 1930L 1 x presion caosa en los miembros sup riores en condicionc normales Rex argent de carliol 17 236 1930c La presion senos en los miembros infenores co condiciones normales en la insuficiencia cardiaca congestia Rex argent de cardiol 17 219 1994 Energy and hydraulic gradient along systemic vens im T Phasol 18 215 EJ TEIN E 1904 Die Diastole des Herzens Ergebn Physiol 3 123 LCLSTEINR 1 WIGGERS CJ AND GRAUTAV GR 1917 Pbasic changes in rafertor cuya flon of atravascular origin Am J Physiol 148 40 EDWARDS 1 S 1951 The effects of lung inflation and epinephrine on pulmonary vascular resistance Im J Physol 167 706 ECDAHL RH 1935 I histological basis of uncontrolled cross-circulation in dogs im J Ihysiol 182 454 EISEWA B AND VIALETTE 19.3 an operitive technique for the construction of venous ales Surg Cinec & Obst 97 731 EPPINGER HI 410 LIOFB4LER L 1911 hreislauf und Zwerchfell Ztschr f hlin Ned 7' 154 FELIX W AVD GROLL H 1933 Die Messung des Blutstromes mit Thermistoren Ztschr f Biol 106'08 1900 Blutstrommessung mit Thermistoren In Compt rend d lle cong angiol Fribourg Elitious universitanes 1956 Euganzende Bemerhnugen zur Bluestsommes ung mit Thermistoren Ztschr f Biol (in press) FERRER MI I HARI EX RMIE SCHNEE M RICHIARD DW JR AVD COLRAAND 1 1943 Hemodynam studies in tricuspid steno 13 of theumatic origin Circulation Research 1 40 FlerscH 1920 Der Einfuss rhythmischer Druchsahu anhungen auf die 11 adderstand sch hultaisse in Geſassystem Irch i dges Physiol 1 8 31 FLEK S 1934 Die lineare Blutben egung und ihre Ozıllation in der Venen ystem Liche f krei laufforsch 9601 FOLKOR B 1900 Ten ous control of blood vessels Physiol Rey 35 629 FRA 186 Ticleaux du laboratoire de Alarey (quoted by Ebstcın 1901) Friv O 1899 Die Benutzung des Prinzips der Pitot schen Rohrchen zur Bestimmung der Blutgeschwindigheit 7tschr f Biol 37 1 1928 Der Ablauf der Stromung geschwindighest in den Gefassen Ztechir f Biol 83 210 ·BIBLIOGRAPHI 133 19994 Zur Methode der Bestimmung der Blutgeschrindug) cit Sitzungslenchte d Cesellsch f Morphol u Physiol in Munchen 34 79 19930 Theorie uni konstruktion cincs optichco Strompeadels Zuschr 1 Bol SS3 19.0 Bermarkungen zu der lbhandlung von Otto Ranke Cber die Registrierung der Strosiung geschwindigkeit us* Ztschus i Biol JB 151 FRAXINI JAND JASKER R 1934 Efierts of rc piration upon the venae cavae of certain martmals as studsed by means of ray cinematography Phycol $1 434 110-1336 Rc piration and the sense llar-further ray cinematograf luc studies J Pliy sal SG 264 1937 4 Monograph op Vcias Springfield Illinois Charles Thomas FULTON JI 1918 Watson mcdicine in its presente asp ct london New Yorh and Toronto Oxford University Presy 19.12 Tesebook or Physiologs I hides 2 and London B Saun krs Co i thod GATER OH HU Rontgenkinematographische Dur tellung ler Fliehkraftwirkung Luitiahrtmc lizin 9 109 19.0 The physiological ellects of prolongrid aceleration In (crman buation Vedline World War II Washington DC Dept of lir Force Tolip 551 Ilexer SP SIELER I O AND WENDT L 1034 The effect of negative pre sure breathing on urine flow J Clin Invest 33 'S 1992 Tolume changes of the left ventricle during blood pooling and exerci in the intact animal Their effects on left ventricular performance Pl y sol Rey 30 143 19b Dic by irostatische Wirkung von Ba lern auf den hreislauf Ein Beitrag zur Isage der Teinin Volument gulation Deutsche Ved J 462 IIENRY II AND IEKER IO 1300 Changes in rentral venous pressure after molernte 1 etnorrhage and transfusion in map Circulation Research "9 ALD SIEMER IO 1936 Iersonal communication GLOVER R P 191 The pre cnt status of intracardia urgers for mitral an 1 aorti steno i Trans and stud Coll Ihysicians P Jadulphua 1 97 19. The technique of mitral commissurotomy In International Symposium on Cardiovascular Surgery Thiladelphia and Lon loa 11 B Saunu rs Co 19 GETZ KI AND Btosz Olsex Ogow Scientitafar--the cir ufation of the strutic South Ifrican M JO 713 19). The gir fíe prollen Timc er 6.) 19 b itchininary obsinations on the circulation in the giraf In Transactions of the Imerican College of Cardiologs New lorh imen on College of Cardiology Sol 5 p 239 Goli bi p r METZNEB JAVO TIE TER KASP H 105, Roatgenlitematographie und Stero skopie in Berlin seit 19.0 Zentralblatt 1 Chirurgie S 401 GOLLANT PHILLIPS R Jr (RATE JT AND Joves RM 1935 Open left heart surgery in dogs during hypothermic asystole with anl without extracorporeal circulation J To Tacic Surg 30 696 GOLLWITZER VEDE K 1932 Vencasystem und Kreislaufre gulierung Ergebn d I hysiol 34 1145 Coltz F A GALE I 18 8 Uber die Drucksert altasse im Inner des Herzens Irch f dges Jhysiol 17 100 GORCOVI BRUNWALD I LD RAVITCA MM 1901 Simultaneous pressure pulses in the human lcft atrum left ventricle and aorta Carculation Rcuearch 432 GORLIN RB 1CW BM BATUES F V SPIEGEL RS AND DE\TER I 1931 Factory regulating pulmonary capillary pressure in mitral stena 15 ln leart J 831 AND DITTER L 1952 Studies of the circulaton dynamics at ret in stral ahte regurgitation with and without steno 13 Ion Licart J 330, GREES II D 1910 Square root extractor Pes sent la truments 1 2 1918 Circulation-blood flow measur ment In Vethods in Medical Research Chicago Icar Book Pulls hers Vol 1 p 66 GRSSG D LAV GREEN II D 1910 Regl tration and interpretation of normal pl a je infly ·131 VEROUS RETURY into a left coronary artery by improsed differential manometric method Am J Physiol 130 114 1918 Thermostromuhr In Methods in Medical Rescarch Chicago Icar Book Pub- Lisbcrs lol 1 p 89 Gross R E 40 IT ATKINS E JC 1933 Surgical closure of atrial septal defects Arch Surg 67 670 Po 1.412 1 4 AND GOLDSVITII E I 1933 I method for surgical closure of interauricular septal defects Surg Cydec & Obst 36 1 GUPIT 1931 Ll ciclo cardiaco consideraciones criticas sobre la interpretacion clásica nuevas ideas obre el mi mo I nyatcly publi lied monograph by Guasp from the Medical Faculty of the Uans crsity of Salamanca Madrid GUITON IC POLIZO D AND ARMSTRONG GG 1934 Vean circulatory filling pressure mcasured immediately after cessation of heart pumping Im J Physiol 179 261 ILADDY I J AD GILBERT RP 1936 The relation of a senous arteriolar reflex to transmural pressure and resistance in small and large systemic vessels Circulation Research 4 23 HALL J T Me Do ALD D LAD WORVERSLE) J R 1932 Velocity profiles of oscillating arterial flow with some calculation of viscous drag and the 'cynolds number J Physiol 128 629 II AMILTON 1 F 19.0 Filling of the normal human heart in relation to the cardio pneumogram and abdominal plethysmogram Im J Physiol 31 712 --- ELLISON RG I ICXERING R LLAGUE E L AND RUCKER J T 1901 Ilemous namic and endocrine re ponses to experienental mitral stenosis im J Physiol 1 6 415 HANSEN I T ESKILD EY P AND GOTZSCHE H 1931 Pressure cures from the right auricle and the right ventricle in chronic constrictive pericarditis Circulation 3 881 ILARKEV D E BLACK II CLLIS L B AND DEXTER L 1904 The surgical correction of mitral insufficiency J Thoracic Surg og 601 1995 The surgical treatment of mitral insufficiency In International Symposium on Cardiovascular Surger, Philadelphia and London WB Saunders Co p 212 HARRISOV TR 1951 Principles of Internal Medicine New York Blaheston Co 2nd ed HARSEY #1628 Exercitatio anatomica de motu cordis et sanguinis in animalibus Frank, furt Sumptibus Gulielmi Iitzeri In English translation by CD Leake Springficld Illinois Charles C Thomas Co 1928 HAYES E W JR DRYDEY P M JASLISOV W L AND BAILEY CI 1923 i nylon cloth oxygenator for extracorporeal circulation Proc Soc Exper Biol & Med 89 413 HELPS E P W AND MCDONALD D 119011 Observations on laminar flow in seins J Passiol 1+ 031 195-1b Streamline flow an eins J Physiol 1965 HENDERSOY Y 1909 Acapra and shock II A principle underlyiog the normal sariations in the volume of the bloodstream and the deviation from this principle in shock Am J Physiol 23 315 -- AND BARRIGER TB JR 1913. The relation of venous pressure to cardiac efficiency Am J Phy 101 31 332 1913b The influence of respiration upon the velocity of the blood stream Am J Physiol 31 399 HENCKLE P J 1 1872 Beitrage zur Anatomie des Menschen mit Beziebung auf Bewegung (Plate VII) Leipzig and Heidelberg Cr Winter (quoted by Rollet 1880) HESBY J P GAVER O AND REETES J L 1906 Esidence of the atral location of receptors influencing urine flow Circulation Research 4 85 AND SIEKER HO 1936 The cffect of moderate changes in blood volume on left and sight atnal pressures Circulation Research 4 01 HOFFMANY W K 1931 Relation of atral info rate to intra atrial pressure gradient during ventricular systole (z v gradient) Am J Physiol 107 433 Holt J P 1910 The measurement of venous pressure in man eliminating the hydrostatic factor 4 J Physiol 130 630 1911 The collapse factor in the measurement of venous pressure im J Phy 610) 184 292 AXD AND ·BIBLIOGRAPHY 133 1943 The effect of positive and negative intrathor3cic pre-sure on peripheral venous pressure in man Am J Physiol i 208 LOLZLON\ER E 1932 Die Volumcaanderungen im menschlichen Thorax wahrend der Herzahtion Zlschr f Biol 92 293 1936 Der itempuls (hardiopacumatische Beregung) und 1 r Blutruchstrom zum IIerzca 7 tschr í Biol 97 403 1938 Dic Stromborste ein elektrischer Geschwindigkeitsmesser fur I lussigkeiten (1 Mitteilung) Grundzuge der Anordnung Ztschr í Biol 93 533 AND STHOVERSTEDT B 1910 Der Strompuls in der Vena jugularis Ztschr í Biol 100 51 Hotssur D I ET AL 19. Lumap I hy siolog New Fork Toronto und London McCraw Il Book Co Inc 2nd ed HCare CA WALTZ It C BRECHER G A PRACLIY J AND HINGSON R 1 1994 Circulatory dynamics of venous return during positive negative pressure re piration Ane thesiology 415 BRECHER G AND CLEXEY L 19,5 Ctrological factors affecting pulmonary artery flow with controlled re piration Surgery 3 215 HUMPHREY, GII VOORE RL AND BARKLEY H 1939 Studies of the jugular carotid and pulmonary pressures of anesthetized dogs during positise inflation of the lungs J Thoracic Surs S 523 HTETLE J 1800 Lehrbuch der natomie des Menschen Wica Wilhelm Braumuller 4th ed JAGER 1937 Venenklappen und Muskelkontraktion Arch f d ges Phy 510138 08 JARISCK 1923 Kreislauffragen Deutsche med Wchaschr 6. 1171 1978 1211 JOCHENI E 1918 Llectromagnetic flow meter In Methods in Medical Research Chicago Icar Book Publishers Vol 1 JONGBLOED J 1931 Observations on dogs with mechanically su tained circulation and respiration J Ippl Physiol s 642 LAGAY 19.2 Dynamic responses of the right ventricle following extensive damage by cauterization Circulation 5 816 I AMS H P 194 Clectronic flowmeter system Rev Scient Instruments 25 201 LLASTROVITZ 1 HUEWITT ES AND LIEBS XOVITZ A 1991 A cinematographic study of the junction of the mitral vale in situ In Surgical Forum Clinical Congress of the American College of Surgeous Philadelphia WB Saunders Co D 204 A LANTROWITZ A 1953 Experimental augumentation of coronary flow by retardation of the arterial pressure pulse Surgery 34 618 KANZOW E 1908 Fortlaufende Messung d horonardurchblutung am uncroffneten Thorax mittels Strom ubrhatheters Tagung d Deutsch Physiol Gesellsch 22 LATZ L N 1930 The role played by the ventncular relaxation process in filling the ventricle Am J Physiol 95 42 AND SIEGEL ML 1931 The cardiodynamic effects of acute experimental mitral stenosis Am Ecart J G 672 LAND KOLIN A 19.08 The flow of blood in the carotid artery of the dog under various circumstances as determined with the electromagnetic filowmeter Am J Physiol 122 788 E B AND CROSS FS 1926 Personnal communication KEMPIL JP KYDD G ATKINSOY JF REED J P AND HITCHCOCK F 1 1952 Effects of po itive intermittent and positive Degatne pressure breathing on dogs Am J Physiol 11 733 HIRLIY J W DOSTANE J W PATRICK RT DONALD DI BETLEL PS KARSUBARQER II G AND W00D EH 1930 Intracardiac surgery with the aid of a mechanical pump oxygenator system (Gibbon typ ) 5 port of cight cawes Proc Staff Meet Mayo CLP 0 201 KLINIECKI A J 192. Considerations Theoriques Sur La Mouvement Des Liquides Dans La Capule De Patot Modifiee Par Cybulskı Essai De Determination De La Vitesso Du Sing Dans Les drteres Compt read Sac de biol 93 83 KOLIV 4 1006 Aa electromagnetie flowmeter Prvaciple of the method and its applicativa to blood flow mcasurement Proc soc Exper Biol & Afed 95 53 ·136 VEVOUS RETURV 1911 An AC aduction flowmeter for measurement of blood flow in intact blood vessels Proc Soc Exper Biol & Med 46 233 1915 in alternating ficld induction flowmcter of high sensitivity Rot Scient Instruments 16 103 1902 Improved apparatus and technique for electromagpetic determination of blood flow Rey Scicat Instruments 99 235 KUSSERON Bh 1955 1 mechanical heart lung apparatus with gas dispersion centrifugal aerator Proc Soc Exper Biol & Med 88 161 LA CR 1900 Iu International Symposium on Cardiovascular Surgery Philadelphia and London WB Saunders Co LAXPORT H 1935 Hemodynamics In Fultons Textbook of Physiology Philadelphia and London 1B Saunders Co 17th ed LANDIS EM 1948 The effects of acceleration and their amelioration In idu ples ja Military Medicine Boston Little Brown and Co Tol 1 Ch 21 p 232 AND HORTENSTINE JC 1930 Lunctional significance of enous blood pressure Physiol Ros 80 1 LASZ L 191 kinematographische Bestimmung der Blutstromung geschwindigkeit in feinsten Gefassen der Conjunctiva und Modells ersuche zur Bestimmung der Grenzgc schwindigkeit welche vom Auge noch als Bewegung wahrgenommen werden hann Helset physiol acta 7 197 AND VULLEN 1951 Uber den Druckverlauf im linken Ventrikel und Vorhof und in der Torta ascendens Helvet physiol acta 955 LALBER II 1928 Untersuchungen uber die Messung der Stromsturhe in Blutgefus.co (1 Mitteilung) Ztschr f Biol 89 217 LAT SON II D BLOOMFIELD R A AND COLEVAND | 1946 The influence of the reparation on the circulation in man with special reference to pressures in the right aurcle right ventricle femoral artery and peripheral veins Am J Med 1 310 LEDDERILO E C 1906 Studien uber den Blutlauf in den Hautienen unter rhy jologi chen und pathologischen Bedingungen Mitteil Grenzgeb Ved & Chirurg 15 300 LED S E CULIVER M M AND STRAUSS SI 1932 Experimental trag po ition of the great vesscls some factors which increase the flow through the atrial septal defect J Thoracic Surg So 612 LEWIS T 1908 Studies of the relationstup between respiration and blood pre «uic J 1 husal 37 213 LIEBAD G 1991 Uber ein sentilloses Pumpprinzip De Naturwissenschaften i 3? 1930 Herzpulsation und Blutbewegung Ztschr í d ges exper Med 19 482 LIGON E NJR 1947 in automatic recording siphon Science 101 6'1 LILLEIJEI CP Corev M HARDEN LAND VARCO R L 1932 The dnect tsion intracardiac correction of congenital anomalies by controlled cross circulatiou Surgery 33 11 READ RC Dell ALL RÅ AUST JB AND ARCO R I 1950 Direct vision intracardiac surgery in International Sympo ium on Cardion cular Surgery Philadelphia and London TV B Saunders Co LED J 11 EGELIUS C AND BOESEY G 1995 Recent developments in angrocardiographs In International Symposiuta on Cardiovascular Surgery Philadelphia and I ondon 1 B Saunders Co LINDGRE. P AND Unhas B 1934 Photoelectric recording of the senous and antcual blood flow Acta physiol Scandinav 32 209 LITTLE R C 1948 The cardiodynamics of tricuspid insuficiency Proc Soc Euper Biol & Med 03 CO2 1949 Volume elastic properties of the right and left atrium Am J I hs szol 158 237 LORTT M L 1867 Recherches sur la vitesse du cours de sang dans les anteres du cheval au moyen d un nousel hemadromographe Paris J B Balliere (quoted by Rollet 1850) LATER R 1669 Tractatus de corde item de motu et colore sanguinis et clısli in cum transitu London Jo Redmayne for James Allestry (quoted from 1 Donograph on Veids Franklin 1937) ·BIBLIOGRAPHY 137 LLCIANI L 1911 luman Physiolog Londoa Macmillan and Co Vol 1 Engl Tran] by F1 Welby LIII1,193 The sali ular dcfects of the left heart I. le urt Baltimore Williams & Wilkins Co, 2nd cl p 17 Lois RheTVEDY J AND BUEU ELL CS 1938 The me Lurement of venous pres sure by the direct method im llcart J 16 67 VHAVE J 190 Ti e study of the pulse arterial bou all at und of the move ment of the hcart Luinburgh and London Young J I entland VEDIE F., IS1Irecis elementaire de Physiologie Paris lol 2 (quoted by Ib to 1001) ALOVET JI JR AD ILAVDFORD SW 1931 Circulatory reg onses to intermittent po i tre and alternating positive negatic pressure respirators J Appl P! 16101 6103 VICOLD D I 1922 The occurrence of turbulent flow in the robit aorta J Physiol 118 310 191 Irterial flow pattern in relation to changes to vascular resistance J Physiol 1° 19. The relation of pulsatile pressure to low in arteries J Physiol 197 533 VELROSE D G 231) heart lung machine for use in mas J Phs 10l 197 IP Vecai EE NonDBURY J W RICHARD AND BURN ELL CS 1932 Studies in er perimental renicarlıl tamponade clfects on intravascular pressurcs and cardiac out put Circulation 6 318 MILSE TIOVOX LV 1930 Theoretical Hydrodynamics New York Macmillan Co MANTER G JA 1933 Re piratory augumentation of inferior casal flow demonstrated by a los resi tance phasic fox mcter im 3 Phisiol 172 416 MONTCO IERY HAD ZINTEL II A 1991 Chnical study and treatment of varicose veins Circulation 10 412 MORTUG`I J B 1 61 Epistola saatomico medica VIT in De sedibus et causia morborum per anatomen indagatis lsbri quinque Ex Typographia Remondituana Venetus (quoted from 1 Vonograph on Venns Franklin 1937) Mosso 15-8 Die Diagnostih des Pulscs Leipzig (quoted by Bohme 19,6) MOTLET II COLEVAND A VERKO L DRESDALE DTBTMXLLSTEIN AND Richards DW. JE 1918 Intermittent porti e pressure breathing JAV 4 139 3-0 MULLER I LAUL AND PIRCLIER L 1918 Uber ein Verbranmanometer mit elektrischer Transmission zur Druck und Geschwindigkeitsmessung Helt phı sol et pharmacol acta 683 19a Uber die Verwendung des Pitot Rohres zur Ge chwindigkeitsmessung Helvet physiol et pharmacol acta 12 33 19316 Über die Verwendung des Castelli Prezıp3 zur Geschwindigkeitsmessung Telet shy sol et pharmacol acta 12 00 MULLER O AND SHILLINGFORD J 19,5 The blood flow in the right atrium and superior vena caya in tricu pi l incompetence Brt leart J 17 163 EALOV T T JA HAFT G J PRICE JE AND GIBBOV JI JE 1950 Pulmonary ventila tion during open thoracotomy J Thoracic Surg 50 66 NEGA IJ 1809 Beitr ge zur kcnatpis der Atnosentrikulachlappes Jes Herzens Breslau Grass Barıh (quoted by Ebstein 1901) VERLICH VE 19.1 Determinants of unpairment of cardiac filling during progres. ite peri cardial efiu ion Circulation $ 377 AEWAY V I STUCKET JE LELOWITZ B S Yotva L 4 DENIS C Tres GORAYTB IJ ZUHDI V KARLSOS I F ADLER S AND GLIEDMAN M 1900 Complete and partial Derfu son of amal und buman subjects with the pump-oxygenator Surgery 8 no NILSSON VJ10 LEVER I 1934 Stromvolumenpulse der herznaben Venen bei yor schuedenan hrei laufzustanden Ztschr i B:of 106 86 OBERDORF I 40 MILCKE O 1904 Untersuchungen uber diciturkung kleiner und mittlerer Stromstarken auf den Kreislauf Ztschr i dges exper Med 124 203 O'NEILL T J E JANTOV O L AND GLOVER R P 1934 Surgical treatment of thicuspid steno 18 Circulation 9 S$1 ·138 VEX OUS NETURY OPDTKE D F AND BRECIER GA 1900 Effect of normal and abnormal changes of intra thoracic pressure on effective right and left atrial pressures Am J Physiol 100 506 VAN NOITE II T AND BRECH£& G A 1930 Further evidence that in piration in creases right atrial inflop Am J Physiol 102 259 AND BRECIER G A 1951 Modifying effects of interatrial septal defect on the cardio dydamics of mitral stenosis Am J Physiol 104 573 PAGE CB HICRAN J B SIEKER HO MCINTOSH HD AND PATOR W 1933 Reflex Venomotor activity in normal persons and in patients with postural hypotension Cir culation 11 262 PAPPENHEIMER JR 1951 Dilferential conductance manometer Rei Scient Instruments 25 912 PETERSOV L H 1951 Participation of the veins in actise regulation of circulation Tedera top Proc 10 104 1992 Certain aspects of reflex and mechanical influences upon venous circulation Federation Proc 11 122 1906 Personal communication PFull W 1929a Die mechanischen Aufgaben das Herzbeutels und seine Rolle bei der Wechselwirkung von intrathorakaler Saugkraft und Herzhralt Anat Adz 67337 1999 Die Herzoberfache und ihre praktische Bedeutung Anat Anzes 20 PIETER II AND WETTEREB E 1033 Strompendel fus elektrische Registrierung der Blut stromuug geschwindigheit (1 Mitteilung) Ztschr i Biol 105 214 Por EUILLE JL 1830 Recherches sur les causes du movement du sang dans les scines J Physiol exp path 10 277 (quoted from 1 Monograph on Icins Franklin 1931) PRAGLIN J AND BRECIER G A 1935 Amplifier for 531 tube bristle flowmeter Re: Scient Instruments 26 385 PURKIVJE JE 1813 Jabre ber d schles Ges i vater! Cultur Breslau p 15. (quoted by Rollet 1880) RASU KIND W D LEWIS D IIIE DERSOY J B HEIMAN D F AND DIETRICK R B 1933 Venous retum is affected by cardiac output and total peripheral resistance Am J Physiol 116 415 REINDELL H WETLAND R KLEPZIG H SCHILDGE E AND MUSSHOFF K 1953 Uber An passung vorgunge und Schadigungsmoglichkeiten beim Sportherzen Schweiz Zt chrf Sportmed 1 97 RussiaGER U 1928 Vatersunchungen uber die Messung der Stromstarhe in Blutgefassen (2 Vitteilung) Ztschr f Biol 88 286 RICHARDS TG AND WILLIAMS T D 1933 Velocity changes the carotid and femoral arteries of dogs during the cardiac cycle J Physiol 1257 RICHARDSOV A W DEMI OY A B AND GREEN HD., 19.2 A benly modified electromagnetic blood flow meter capable of high fidelity Dow registration Circulation 6 400 RODBARD AND Hatz L N 1952 The neurogenic control of the blood vessels Circulation 12 448 ROLLET 1880 Physiologie der Blutbewegung In Handbuch der Physiologie Leipzig FC Togel Co Tol 4 p 146 RO EJC Costa S J JE HOFYAGEL C AND MASSELLO EA 1992 The effects of exclusion of the nght ventricle from the circulation in dogs J Clin Invest 34 16% Rost E JR 1932 Beitrag zur kenntaus der Kreislaufverbaltnisse bei lederbelebung durch Veranderung des intrapulmonalen Druckes Ztschr ges exper Med 8293 RUSINER R F BECEMAS F L AND LEE D 1947 Protection of the cerebral circulation by the cerebro pinal fluid under the influence of radial acceleration Am J Phyol 161 355 CRTSTAL D K AND WAG\ER C 1993 The functional anatomy of ventricular con traction Circulation Research 1 162 1951 Shrinkage of the heart in anesthetized thoracotomized dogs Circulation RC search 2 22 19:52 Applicability of Starlings law of the heart to intact unapesthetized annals Physiol Re: 95 138 1935b Length-circumference relations of the left sentncle Circulation Research 9 69 ·VIDLOGNAPIS 139 Sursorr S Jana BERGLVD L 1927 Pressure volume characteristics and stress relaxation 22 the pulmonary vascular bed of the dog Am J Physiol 171 238 SCHER & MESGERT TII AND Young IC 1953 Compact flowineters for use in the unanesthclized anual an electronic ver con of Chauveau s hemodrometer Science 118 $2 SCHUBETE EL 1817 Physikalische Croreningen uber den Krei lauf des Blutes und uber die Inraíte welcbe ibo her orbriages Gilberts Aznalen der Phyesh Neue Folge 27 40 (quoted by Ebstco 1901) SCELT N D 1918 Dynamic effect of inspiration on the simultancous strobe volume of the nght and left ventricles Am J Plisso! 164 2.3 SEC.KURT E EAD BRECHER GA 1950 Splachdac hemodynamics and asigca utilization during hemorrhagic shoch Cuculation Research (Submitted for publication) SEAB T Ano kisi 1933 Iceous pressures Japan J Physiol Soc 18 8 SHAFFER B SILDEN CAND LATZ L N 1031 Observations on the interafrial pres suse gradients in man Circulation 10 527 SHLEY R E GREGO DE AND SCHROEDER ET 1913 An experimcata) stult of low patterns in various pempherni arteries tm J Physiol 198 718 Sutter R I E 50a C GartNG RE Voss # G AND JOHNSON I 1942 The differen tial effects of respiration on the left and nght ventricles im J Physiol 15" 620 SSOSTRAND T 1903 lolume and distribution of blood and their sigo:ficance in regulating circulation Inn Re Phyeol 33 702 SYTE EL HILGOS RARANDALE RW AND JEFFERY GA 1952 Hemodynamic changes result.og fram losertion of a rolameter in the enous circulation of a dog Texas Rep Brol Med 10 64 SPENCER VI I AD Devtsov AB Je 1955 Measurement of blood flow through intact vessels with the square male clectromagnetic flowmeter la Comptes redu du IIe cong Angol Inbourg Editions usis ersitaires AND m. 1996 l hasic for relationships in the aorla led Proc 10 1 6 STRAD U 1910 The diastolic filling of the mammakaa hcart J Physiol 40 3.8 mam 1973 Die Bestimmung der Ge chwindigkeit des Blutstromes Ibderhalden E Handb Brol Arbeitsineth Abt v Teil 4 I kreislauf u Atmung 1 479 1996 Die Dynarosh des Terzens la Handbuch der portalen und pathologischen Physiologie Berlia Bcthc-v Bergmann Tol 7 p 237 Sway IG MOVSGOMERY A V DAVIS I CJR AND MICKLE E R 1950 toethod for rapid measurement of intrarcnal and other tissue pressures J Exper Med 9? G'S TAASHIMA NI 1933a Experimental and closcal study of venous retura Part 1 Relation shup beeseen cardiac s stole and crous return fap Circulation J 17 309 in Biol Abst 99 280.6 1904 19036 Clinical and experimeatal steely on vedous return II III Influence of pneumo thoraces og vchous return Jap Cuculation J 12 3 8 In Biol Abst 28 23?10 10+ 194 c Clinical and experimental study o 1 CROUS returs IV V Influence of respira tion on cnous returu Jap Crrculation ) 17 391 La Brol Abst 29 23211 2954 1954 Clinical and experimental study og enous-return VI Influence of change of posture and exercise og enous return Jap Circulation J 17 474 In Biol Abst 13 TAIVO V 191 Reflex cardse acceleration by simulation of the receptor area of the pulmonary seins and their vicinity in the left atriun Nippon J Asgio Cardiol 15 1 IQ Biol lbst 26 3608 1952 TIGERSTEDT N 1921 Die Phy islogie des Kreistsufes Berlo and Leipzig Walter de Gruyter and Co Vereinigung wisseaschaftlicher Vesleges SERDADZ C 1848 Die Lrscheinungen und Gesetze der Stromgeschiwadigkeit des Blutes I rankfurt (quoic by Rollet 1850) VILLA L 194 Passivite cu activate diastolique? Sera hop Paris su 617 OLANEX 1 W 1850 Die Ilamodsaamik Leipzig Breitkopf and Inertel IDLJITIO P P IVOODBCAT B A 10 Astes B E 1914 Influence of different forms of mechaneal brificial respiration on the pulraonary and systemic blood pressure JAM 1 73712 1951 106 1066 ·1410 SEVOUS RETUR TOS DES ILLES N 1906 Tersuche uber die Saugwirkung des Herzens atschir Pathol u Therapie 3432 TOY ILALLER | 1803 Irrst lines of Phy hology Troy Obadial I enniman & Co Tran I from 3rd Latin cd Ist Amer cd 11 AGOSER G TY AND LIVINGSTON 1 C 1928 Ipplication of venturimeter to measurement of blood flow in ves els J Pharmacol & Exper Therap 32 1.1 11 ARDEX HERE RCDL WALL RI Ilse J B Court M ZIEGLPR R. 1 ko RL AD LILLEBEI C 1 1995 Direct VISION intracardiac surgers by means of a rescrioir of arterialized venous blood J Thoracic Surg 90 619 WATKINS H L JR AVD Gross R E 1930 Lrperiences with surgical repur of atual septal defects J Thoracic Surg 30 469 VATROLS W GDAUS LAND ADERSON BV 1900-51 Manunlls assisted and cou trolled se pnation its use during mhalation anesthesia for maintenance of Dear normal physiologic state rey let Incsthesiology 11 61 1090 and 1 33 1911 WEDEVEYER G LHC 1878 Untersuchungca uber den hrei lauf des Blutes und insbeson dero uber die Bewegung dessclben in den Arterice und Capıllargelassen mit erhlarcnden Hindeutungen auf pathologische Erscheinungen Hannoucr WETTERER [ 1937 Eine neue Vethode zur Registrierung der Blutstrumung geschwindig hcit am uncrofincten Gef 153 Ztschr f Biol es 26 ----- AVD DEPPE B 1939 Vergleichende tserexperimentelle Votersuchungen zur physikal ischen Schlagvolumcabestimmung (2 Vitteilung) kaninchen und Kuntzen Ztschr í Biol 99 320 1910 Quantitative Bezichungen zwischen Stromsturke und Druck im naturlichen Kreislauf bezcith h variabler 1 la tizitat des arteriellen Windhcoscis Itschirf Biol 100 200 1934 Flow and pre sure in the arterial system their hemodinamuc relationship and the principles of their mcasurement Minnesota Med 3 17 WEYER R 190 Die I crteilung des Durthermie-Stromcs im Blutgefuss bei der Thermo stromuhr Vessung Irch f d ges Physiol 262 1 -- AND CHOFF J 1936 Durchflussme sung mit der Diathermie Thermostromuhr bei pulsierender Stromung Erch I dge Physiol 20" 152 TWITTENBERCER J L 1903 Irtificial respiration Phs $101 Rey 37 611 TicgERS C J 1914 The nature and causes of the respiratory pressure variations in the pul monam artem Im J Physiol 30 124 AND FEIL I 1922 Cardiodynamics of mitral insufficiency Heart 9 149 1998 The Pressure Pulses in the Cardiovascular System London Aex Jork and Toronto Longmans Green & Co 191" Peripheral circulation Inn Rer Physiol 3 235 LEV V V AND GRAHAM G 1917 Regional intrathoracic pressurcs and their bearing on calculation of effective enous pressures Am J Physiol 151 1 1920 Physiology in Llealth and Disease Philadelphia Le Iebiger 5th ed 1992 Circulatory Dynamics New York Grunt & Stratton 1951 Spezielle hamodynamische Gesichtspunkte experimenteller licralla penichler Verhandl d Deutsche Ges f kreislaufforsch 29 3 WORMERSLES JR 1935 Method for the calculation of u clocity rate of flow and uscous drag in arteries when the pressure gradient is known J Physiol 127 553 LAMPADA S AND BCATOY A C 1934 Effect of reduced tissue pressure on blood flow of the fingers the veni asomotor reflex / topl Physiol 6501 Yu P N LOLEJO1 F Ja., NJE R E JR Joos II A BCATTY D C AND MAHOVET L B 1951 Changes in pressuies in the left atrium and pulmonary artery immediately before and after mitral val uloplasty New Lagland J Med 21 "64 LIESKE H JR BAR T D AND LEVY MI N 1905 sensitase optically recording mechani cal balance Proe sot Exper Biol & Med $61 ZCCEABL HLER 1815 De motu sanguinis per scoas y general de medecine 33 (quoted by Ebsteia 1901) ·Index Acceleration factor causing artifact in Nox curic 441 9 Iceleration positive effect of on cerebral sinus pre surc 66 cffect of on enous return 16 frets cholinc (sec Cholinergic) Idrenalin (see Epinephnne) Idrenergic stimulation of vasculature 21- Inalogues used for flow and pressure studies 62-64 CS 0 115-116 Iue the 12 affecting circulatory conditions 3191 Inticoagulants u cd for flow measurements 49 1pcs movement of 4 1. Dea era con tincy of flow during 9 Au totle 3 Irteries changes in cross-sectional area of 34 li tention of 16 3? 41 flowincter introducing re i tance to flow in 32 płasic flow reserval during cardiac cycle in Itros entricular pre ure gri lient in mitral stenosis 118 in pericardial cffusion 120 in tricu pod stenosis 118 trio entricular ring counteracting of te gurgitation by contraction of 116 Itrium 1 piration by dintole of 2 inflou into 9-10 11-1.0 124 pres urcs in 5 18 26 23 71-90 116-120 reservoir function of 101 Izygos factor determining blood flow in op en er liotomy 1 6 presures affected by artificial respiration in 93 93 rigidity of walls in 6 32 volume flow through 26 intcrroleg construction of 11 21-23 re istance of 26 57 Artificial respiration 79 91 107 affecting 1 enoug return 6 91-107 wffecting enous return and cardiac output 97-08 by po ituvc pre-sure lung inflation in the closed chest J3 in the open chest 81 97 Hy intermittent positive begati e pre sure respiration in tlic cloned clct 93 in the open che t 93-97 Atrial fibrillation effect on flos in central eins 103 Bich flon (sce i nic blood flow rey crsal) Bernoull effect 57 Blood depots gencral 22 intrathoracic 24 Bloolflos arterini effect of collap c und wall ugidity on 26 measurement of 29 recording of with bristic flowmeter 46 9 100 110-117 recording of with electromagnetic j endu lum 41-43 retcrsal of during cardiac cycle 41 effect of longitudinal pressure gradient on 11-12 23-26 cffect of scssels radius on 11 effect of viscosity on 11-1" recording of flow rate of 0 42 102-114 Blood sou venous computation of flow tracing 40 during cardiac surgery 121-127 during depleting and collapsed stages 62- 64 0-1 dy pamics of 19 perus beral circulation 61-62 effect of collapse on 9-96 516 effect of ventricular contraction ? 101- 107 inethods for mea uremcat of 1 99-53 necesitz for direct measurement of 28-29 phasic changes of 3 102-114 quantitation of u ciersal during cardiac cycle of 105 113 i rough lis er 83-81 Velocity of 6 27 101 without salte 67-69 Blood infu 100 for maintenance of con tant circulatory conditions GO 79 123-126 Blood resort ours 2? function of central seins 1101 Itrial systole flow reduction in central seins during 10% flon rever al in central veins during 101 hemodynamic function of 113 Itrial sell operation for repair of interatrial septal defects 123 ttroventricular junction movement of 4-6 105-107 109 141 ·142 I\DET 46-41 Blood reservoirs Continucd fluctuations of 29 intracardiac 24 112 gradient of 57-59 intrathoracic 21 Cerebral circulation maintenance of 66-67 mobilization during artificial respiration of Cerebral sinus pressure in 66 101 Chatter of veins 62 splecn acting as 24 Cholinergic stimulation of a culature _", Blood Olumc 24 59 Circulator collapse ( ce also shock) u? Brads cardın Circulatory dy anglics general 2 59-190 in hypothermia 123 during cardiac surgers 121-127 enous return affected by 107 Juring pericardial cu jon 119-190 Bristle flow meter 43-7 in the presence of heart valse lesions 115- calibration technique 17 119 mechanoc lectronic transducer *0734 used Circulatory regulations 21 in 43 Circulatory re eric 24 101-10" 121 modified type of 97 Closed chest venous return in 1140 in measuring cardiac variations of se cardiac variations of 108 nou return 102-114 eficct of intermittent po itse regatne pres ure lung inflation on 91 92 9--98 Calibration of flow meters Effect of natural respnation on -2-70 S- «9 81 lıncar 4° nonlinear 40 47-48 cffect of positive preure lung inflation on 91-95 9 -98 technique of 47 Cardiac output Closed herrt surgery problems of venous fox in 121-123 alteration in 23 direct recording with bristle fowmeter of Collap e chamber as venous counterpart to arterial compression chamber 113 dynamic imbrance of 23 Collapse of essels cffect of central venous reservoir pressure ab ence in congestive fazlure 90 compared to collap c of rubber tubes 62-6 on 28 complet 51-57 59 maintenance at fast heart rates 208 measured simultaneously with venous re counterforce preventing (6-67 during extracorporeal circulation 12. turn 04 reduction with artificial re piration 101- flow measured during 60-62 in different regions of extrathoracic eins 102 86 relation to 1 enous return 21-23 110-112 sudden lacrerse of 22 influence of 10 ziration on 71-102 intermittent 61 123 Cardiac surgery effect on cnous return 121- partial 57 56 59 127 Cardiac lie lesions hemodynamics of 115- siguificance in peripheral circulation 65--0 terminology of 59 119 time factor affecting -0-11 Cardiac uerations of venous flow 8-9 102- two stage ploce in olcd la 62-63 Cardio pncurnogram systolic ventricular suc Collapse theory 9 27 -3 tion revealed by 4 Collapsed stage of veins Cardiotomy joblems of vcnous return dur effect of lux perolemia on $? ing 193-19 cffect of hy povolemia on 81-82 Catheter flowmeter effect of the negatne phase of artificiu Pitot type 38 91 re Paration ou 93 Thermostromuhr type 50 as related to respiration #1-10? Cathcterization studies 118 time factor ficcting "1 Caval band affecting flow in inferior cna Commissurototy 118 cara -8 82 Compliance delayed 21 Central caous flow Compres lon chamber 41 11. as related to pressure gradient 57-29 Conge tion of seins 62 193-194 phasic changes of 7 101-107 110–112 Controlled re piration (sec Irtificial 16 pira Central venous presure general 21 tien) ·INDEX 13 Counterforce resenting venous collapse Gom Croucirculation in canac surgery balancing of coous return dunibg 191-123 controlled 121-126 vocagtrolled 124 Cromectrocal area of scesel con tancs of for fox racasurements 32 dynamic ehwages of 59-65 fixation of 39 13-11 17 Cumularne recording of blood flow 30 GO- 61 191-122 Electronic Dorse limstation of Sowmeter sensitity by 10 signal to DOLE mtio 13 Esdotracheal psex ure venous retur fected bs changes its -100 Loers conscrvot af linetic ioto potcoto] 34 00 5 kunctie w 41-7 J7 potential 30 5 Lpinephrinc rection of seins to 2 Excrcise cacet on blood renoirs 3 Espiration affecting caous blood flos &9-03-6 Extracorporcat circulation problems of Ichou. return in 1981 Damping of pulsatie kon 30 Depleting stage of seid general 69-63 70 effect of hyper olema on $2 cicct of by por olema on 81-82 c&ect of the digatise phase of artificial respiration on 33 43 related to respalon 7l-102 time factor affecting 71-2 Diaphragin muscle contraction of 83-84 moi encat affecting venous return 6 79 aplancter action of 8-79 Diastole atrial 23 Diastole vcntrcular 2-3 Acceleration of cogus flow during 107 actise muscular expansion during 23 deceleration of venous Hos during 28 32 elastic recoil during 3 110 expansion of coronary vesscla dundg 3 Euchug action of 3 28 110 Diastolic ventricular filling acture 110 148521 e 28 110 problems of 2-3 28 110 Differential pressure flow meter general 34- 41 calibration of 40 critique of 40-41 fidelity of 33 resistauce to blood Sow sptroluced by 32 Diferential presure manometer 37 Electrical transmission for 39 Iisustations of optically recording 9 Tracple of 39 Di C05102 arterial 16 39 41 atral 89 108-109 Mezous (see Venous distension) enricular 105-109 Don lers clasical theory of thoracic sspusa to 9 7 2- 3 Lalema orthostatic 20 El torat res tance di anges utilized for blood flow recording 42 Factor of salets for mantenance of sezous return 125 Taunting cuved bi po itse acceleration 16 ortho tata 15 21 Femoral venous pressure afieeted by spontaneous re piration 82 luting in.piration 81 Filtration bs pressure gradieat scroes verzous and capillary walle 20 Flow measurement critique of 40 dunog atmo phone pressure in auays 93 of enous blood i 13-30 with differential pressure dowmeters 361 Flowmeter 30-51 bristle 43-47 83 91 on tle tachograph 42 catheter & 91 catheter therzaostromuhr 0 diatberms thermo tromuhr 50 differential pressure #1 electromaguetsc 34 41-449-30 electromagnetic pendulum 43-43 Electrošaric 51 hemouronograpb 42 pendulum 41-49 strain gauge 41 tambour 31 60-81 thermistor 52 Thermo tromuhr 20 Flor pulse 36 Franh Otto 3 32 33 41 42 49 Frequenes of response bristle flowmeter 4a 8 diferentai manometers 39-40 Electromagnetsc fowmeter vo How mcters 39 manometies 32 relation to sensit2t) 40 ·141 IDI relation of central chous pressure to 69 relation of right ntrial pressure to 2-6 alıcs in girne 67 sencsection of cxternal 39 Juer bloo 1 flow through 83-81 Lung inflation (sce irtificial ic piration) I ungs effect of clistic traction on atrul and icntricular filling 6-8 Galen of Pergamon 2-3 Giraffe maintenance of circulation in head of 67 Gollutzer Veer hlothilde 9 83 89 von Huller Albecht 2 8 Harici Sir William 1 106 Henrt (sce also Cardiac output) 11(eleration of 24 107 acceleration of sedous blood flow toward 2 augmented output of right 98 blood flow from 1 27 46 110-112 blood flow to 1 27 46 102-114 decieasc of right heurt output during lung inflation 102 impairment of right herrt filling 99 mcchinism enabling rapid filling 22 110 1CCT OIT function of 23 Jesidual volume 23 109 elf regulator mechanism of 101-108 Hcurt action effect of on caous return 1 27 101-114 Heart fulure 8 cffect of resition on right 90 Hemodinmis 11-14 cffect of pendulum flow meter on 49 in enou Item 25 51-57 HIepirin (ce Inticoagul ints) Homeostale 21 28 Humoral regulation of venous tone 21-24 Hi Irostatic pres ue 13 16-20 6 Ilypothermia 18 used in open heart surgery 123-124 Hicri olemı ( also enous plethoia) enou retuin in state of 82 89 Hyposolcmia venous return in state of 8? 95 102 Minomctci condcn cr differential 6 differential 37 diffciential conductance 39-10 clectrical diffcicotia 39-10 miniature 59 optical 38 Manometrs physical principles 3 5 3? Vean flow accordcrs 31 Mechanoclcctric trans lucer #5 34 43 Mitral in ufficiency effect on va nous return 113-11. subscal correction of 116 Vitral teno esluit on cnous return 118-119 surgical correction of 118 Mullci s experimcat 71 72 SG 83 Muscle pump alies nding 19-20 without valses 0-0 Myocarduum cntriculir competente in fav pothermir 123 contraction providing 2 19 a fronte 16 101-107 112-114 Vervous regulation of chou tone 21 24 Normoi olema cnous return in state of Si 91-95 In putin influence on venous bloo 1 flow 9 ? .1-102 110-112 In uffidcncies of atrioventri ular values 115-11" sugicul collection of 20 116 of venou valses 20 Integration of flow tracing 40 tu 99 Interatri l septal dcfert (sperimental for relief of pulmonary ve nous congestion 118 i pur of 199-123 hunt flow through 122 Interco til mu cles iction on nous return 9 Intrnca limc uirgery 1'1-1 7 Jugular vein citernal 86 Pres vc mca urement in 60 pulsatile collap in 9 66 Open chet effect of pontaneous re pirators attempts on renous icturn in "6 81 cficct on pres ure gradient between extra thoracic ca els ind heut 7 SI failure of flow incron e by intermittent positis e negative pre uc re piration in 97 po itnic preliic lung inflation in 9 9. Juſt of blood 1c eri oirs because of 23 191 enous return in 91 93-97 9 100 101-109 Open heart surgery problems of venous flow in 123-127 O cillations of cou presne unr litcu to hcart rate 6G Os er hoot ja flow curves 3% 43 Ougenation of bloo I during our liac silrgery 126–197 ·I DEL 140 Pericarditis con Incine affccting enous re turn 119 Fericardium effect of removal on cous low 103-106 tamsons le bs (ffu ion of 115 119-120 Icripheral cnous flow foo I cripheral senous pressure 62-63 Phisic bloo I flow it tcncg 41 recor ling by Liri tle flowmeter 46 rior ling by clectromagneti flowmeter 49-50 recording by bcmo Iromograph 4? I hisic blood flow rever al during cardiac cycle in arteries 41 in presence of tricu pil insufficiencicg 116– 11/ recording with bristle flow meter 46 recorling with differential flow meter 41-42 recording with electromagnetic flowmeter 41-42 in vein 105-106 113 visualizatın 52-33 Phlcbostatic levcl 19 Il repicotomy cffect on inferior caval flow 79 1 slots cffe t of a clcration on 16 pies ure suits u ed by 16 I stotinct ro- 1 ln mi volume control of 24-25 Plethy mogruphy u 90 Poivuilles Law 11 13 no liatin for tube with ellipti ros eotional ure 9 51 Pooling of tool in gracial 21-23 in the nortalin 84 Portal circulation flow li namics of 83-81 repertoir fun tion oí 24 lotion effect on (Dou di tension 17-18 22 cffcct on enous return 15 22-23 Pressure atmo plcric as referenre lsel 13 62 66 atmo The onuyc of venous compres ion (collaj Sc) 1,-18 60-62 68-10 Atmo i hrie in artificial e piration J1-102 CFT (tie 13 extra scular 13 62 66 67 hy dio tatic 13 16-18 intra ab lominal 9 -8-84 satrathoracic 5 9 13 71-102 intravasculai 13 17 62 66 lateral 12 ret 13 tixue 13 66 8 tran mural 13 62 107 110 I re ure flow re istance relation in eine 39-60 I tesure gradient acro's ieswel wall 13 along cuatril velns a -59 along vascular beu 13 18 alternatigas affecting olume flon 68-70 in artericg 26 atrioventricular in mitral and tricuspid stenores 118 bctucen per heral and catral veins 26-27 compensatory rise in 101 rclation to flow during re piration (1-102 Sarations affecting flow 59-65 in seins 26 Pres ure mea urement strial 5 118-190 limitations for cu aluation of blood flow i 28-29 53 principles 12-14 relation of blood flow to 62-61 1-102 Dous 15 Prre ure pump hcart acting as 21 106 Pressure suit ue by pilots 16 Pulmonary artery blood flow measurement 9 97-101 Pulmonary vascular bed reflexes elicited by chlatation of 24 re croir function of 22-23 te i tance of 10 9-100 110-112 Iulmonar) cins 113 Pul atile collapse of vein 8-9 €66 123 I ulsatile flow in cine 9 31 effect of long tulong on of cffect of partial collapse on 67 65-66 unrelat I to heart a tion or respiration 8-9 60-66 Pulsatile flowmeters 0-51 Pur owgenators for ardiac urger 16 I urhinje Jan Liang ta 4 מן Kite recoiling of blou i flow 30 11-112 1 4 Receptoi pon ling to stretch in enous wall 94-23 R flere ilrenciguc 52 axon 23 Bainbridge 113 Liolin rgic 22 clicited by pulmonary venous dilatation 4 clicite 1 by stretch receptors 21 pressure reflex 91 24 seni a omotor (Burton) 23 veno venous (llesand r) 24 Regurgitation in mial and tricu jilinsuffi Cicacies mechanı my counteracting 115- 116

·148
IDEX
Tcnous return-Continued
lag of venous retum in systemic cins 23
relation of to aortic pressure 93
relation of to homeostatic mechanisms 28
Venous tone 21-22
Venous values 19
Teatricular diastolc (sce Diastole)
entricular filling
effect of vcntrcular diastolc on 28 103-
Ventricular sy stole (8cc Systole)
Yentricular Yolupe (sce Rc dual volume)
Vertebral veins fon through 66-61
113 a fronte general 2 57 101-107 112-114
during ventricular diastole 24 109-110
during ventricular systole 3-6 101–10,
112-114
19 a tergo 1-2 57 112-113
Volume clasticity 12
olume llos (sce Blood flow)
110
in mitral and tricuspid stenoses 118-119
Ventricular suction
during diastole 28 109-110
during systole 27-28 32 101 107
ray cincmatography ix 5 17 27 39 51 53
Zero flor 30 47

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